Ignet

Gene Information

Gene symbol: ITGB2

Gene name: integrin, beta 2 (complement component 3 receptor 3 and 4 subunit)

HGNC ID: 6155

Synonyms: LFA-1, MAC-1

Related Genes

#	Gene Symbol	Number of hits
1	CD14	1 hits
2	CD2	1 hits
3	CD4	1 hits
4	CD44	1 hits
5	CD68	1 hits
6	CD80	1 hits
7	CD86	1 hits
8	CD8A	1 hits
9	COL1A1	1 hits
10	COL1AR	1 hits
11	CRP	1 hits
12	EDA	1 hits
13	FPR1	1 hits
14	HLA-A	1 hits
15	HMGB1	1 hits
16	ICAM1	1 hits
17	IL1B	1 hits
18	IL6	1 hits
19	IL8	1 hits
20	INS	1 hits
21	ITGA1	1 hits
22	ITGA4	1 hits
23	ITGA5	1 hits
24	ITGAL	1 hits
25	ITGAM	1 hits
26	ITGAX	1 hits
27	ITGB1	1 hits
28	KRIT1	1 hits
29	NEUROD1	1 hits
30	PPARG	1 hits
31	S100A1	1 hits
32	SELL	1 hits
33	SELPLG	1 hits
34	SSR1	1 hits
35	TDGF3	1 hits
36	TGFB1	1 hits
37	TNF	1 hits
38	VCAM1	1 hits
39	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	1340530	The blood monocytes adhere to endothelial cells unstimulated and after stimulation by interleukin-1, tumor necrosis factor or other mediators.
2	1340530	E-Selectin (ELAM-1), P-Selectin (GMP-140) and receptors of the immunoglobulin superfamily (ICAM-1, ICAM-2 and VCAM-1) are expressed on endothelial cells in basal conditions and after activation.
3	1340530	As estimated by flow cytometry CD11b/CD18 expression on diabetic monocytes was increased.
4	1340530	Pentoxifylline reduced CD11b/CD18 expression on normal and diabetic monocytes.
5	1340530	The blood monocytes adhere to endothelial cells unstimulated and after stimulation by interleukin-1, tumor necrosis factor or other mediators.
6	1340530	E-Selectin (ELAM-1), P-Selectin (GMP-140) and receptors of the immunoglobulin superfamily (ICAM-1, ICAM-2 and VCAM-1) are expressed on endothelial cells in basal conditions and after activation.
7	1340530	As estimated by flow cytometry CD11b/CD18 expression on diabetic monocytes was increased.
8	1340530	Pentoxifylline reduced CD11b/CD18 expression on normal and diabetic monocytes.
9	1673028	Expression of a soluble and functional form of the human beta 2 integrin CD11b/CD18.
10	1673028	Furthermore, murine monoclonal antibodies directed against the CD11b/CD18 (CR3) heterodimer have been shown to reduce, by 50%-80%, phagocyte-mediated ischemia-reperfusion injury in several organ systems, such as the myocardium, liver, and gastrointestinal tract and to inhibit development of insulin-dependent diabetes mellitus in nonobese diabetic (NOD) mice.
11	1673028	Expression of CD11b/CD18 in a soluble and functional form might therefore be potentially useful as an anti-inflammatory agent.
12	1673028	Expression of a soluble and functional form of the human beta 2 integrin CD11b/CD18.
13	1673028	Furthermore, murine monoclonal antibodies directed against the CD11b/CD18 (CR3) heterodimer have been shown to reduce, by 50%-80%, phagocyte-mediated ischemia-reperfusion injury in several organ systems, such as the myocardium, liver, and gastrointestinal tract and to inhibit development of insulin-dependent diabetes mellitus in nonobese diabetic (NOD) mice.
14	1673028	Expression of CD11b/CD18 in a soluble and functional form might therefore be potentially useful as an anti-inflammatory agent.
15	1673028	Expression of a soluble and functional form of the human beta 2 integrin CD11b/CD18.
16	1673028	Furthermore, murine monoclonal antibodies directed against the CD11b/CD18 (CR3) heterodimer have been shown to reduce, by 50%-80%, phagocyte-mediated ischemia-reperfusion injury in several organ systems, such as the myocardium, liver, and gastrointestinal tract and to inhibit development of insulin-dependent diabetes mellitus in nonobese diabetic (NOD) mice.
17	1673028	Expression of CD11b/CD18 in a soluble and functional form might therefore be potentially useful as an anti-inflammatory agent.
18	2250718	Insulin-dependent diabetes mellitus (IDDM) is a disease with an autoimmune aetiology.
19	2250718	The monoclonal antibody 5C6 is specific for the myelomonocytic adhesion-promoting type-3 complement receptor (CR3 or CD11b/CD18) and does not bind to T cells.
20	2261508	These molecules responsible for leukocyte adhesion are heterodimers consisting of a common beta subunit and different subunit CD11a/CD18 corresponding to LFA-1; CD11b/CD18 to Mac1/Mol; CD11c/CD18 to GP150-95.
21	2261508	Cytokines such as IL-1 induced the expression of ELAM, increased the number of ICAM and Human Leukocyte Antigens (HLA) DR, DP, DQ.
22	8405709	In IDDM, mononuclear cells accumulate in the islets of Langerhans and destroy insulin-producing beta-cells.
23	8405709	The cell line was uniformly CD4-positive, TCR V beta 5.1-positive, LFA-1-positive (CD 11a/CD18), VLA-4 alpha-positive (CD 49d), and CD 44-positive but negative for L-selectin (peripheral lymph node homing receptor).
24	8899799	Appearance of cells expressing CD80 and CD86 costimulatory antigens in the pancreas of nonobese diabetic mice.
25	8899799	The immunoregulatory effects of the costimulatory CD80/B7-1 and CD86/B7-2 antigens expressed by the antigen-presenting cells may be crucial for the development of immune responses and their absence may lead to clonal anergy, which is important in the prevention of autoimmune reactivity.
26	8899799	To evaluate the role of the CD80 and CD86 antigens in the development of insulin-dependent diabetes mellitus, expression of these antigens in the pancreas of normal and nonobese diabetic mice was studied.
27	8899799	The pancreata of normal BALB/c mice and young nonobese diabetic mice contained no CD80- or CD86-positive cells.
28	8899799	CD80- and CD86-positive cells appeared in the pancreas of nonobese diabetic mice by 6 weeks of age.
29	8899799	Double immunostaining at the age of 12 weeks showed that CD80-positive cells accumulated around the islets of Langerhans but no insulin-containing cells expressed the costimulatory molecules.
30	8899799	The morphology of the CD80- and CD86-positive cells was heterogeneous.
31	8899799	Many were Mac-1 integrin (CD11b/CD18) positive, suggesting that macrophages expressing the costimulatory antigens are present in the pancreas of all nonobese diabetic mice by 12 weeks of age and that CD80- and CD86-expressing macrophages may be involved in the local regulation of antiislet immune responses.
32	9075429	Expression of CD11b, CD18, and L-selectin was measured on granulocytes and lymphocytes in whole blood within 1 hour of blood collection.
33	9647438	Serial frozen sections of grafts and controls were stained by immunoperoxidase for rat MAC-1, class II MHC, CD2, CD4, CD8, B-cells, VLA-4, LFA-1, L-selectin, ICAM-1, and VCAM-1.
34	9647438	Third, the second wave of lymphocytes arrived from the renal parenchyma to form a dense band at the graft-kidney interface and around grafts by days 4 and 6 (allo >>> iso); CD4+ cells vastly outnumbered CD8+ cells, with CD4+ cells being mobilized first and from interstitial vessels throughout the entire kidney.
35	9647438	Large numbers of L-selectin+, VLA-4+, and LFA-1+ cells were seen in the infiltrates with the most intensely staining cells being intravascular.
36	9647438	Endothelial staining for ICAM-1 and VCAM-1 was prominent throughout.
37	9647438	Both class II MHC and ICAM-1 expression were induced on renal tubular epithelial cells, but neither was found on islet parenchymal cells.
38	9647438	Serial frozen sections of grafts and controls were stained by immunoperoxidase for rat MAC-1, class II MHC, CD2, CD4, CD8, B-cells, VLA-4, LFA-1, L-selectin, ICAM-1, and VCAM-1.
39	9647438	Third, the second wave of lymphocytes arrived from the renal parenchyma to form a dense band at the graft-kidney interface and around grafts by days 4 and 6 (allo >>> iso); CD4+ cells vastly outnumbered CD8+ cells, with CD4+ cells being mobilized first and from interstitial vessels throughout the entire kidney.
40	9647438	Large numbers of L-selectin+, VLA-4+, and LFA-1+ cells were seen in the infiltrates with the most intensely staining cells being intravascular.
41	9647438	Endothelial staining for ICAM-1 and VCAM-1 was prominent throughout.
42	9647438	Both class II MHC and ICAM-1 expression were induced on renal tubular epithelial cells, but neither was found on islet parenchymal cells.
43	10206487	The role of CD8+ cells, cell degeneration, and Fas ligand in insulitis after intraperitoneal transfer of NOD splenocytes.
44	10206487	Cells expressing CD4, CD8, CD18, CD49d/CD29, CD44, CD54, CD80, CD86, CD106, CD11b/CD18 or DNA breaks were stained in the pancreases of female or male scid/ scid mice after adoptive transfer of lymphocytes from older than 12-week female nonobese diabetic (NOD) or Balb/c mice.
45	10206487	After intraperitoneal adoptive transfer of NOD splenocytes to female severe combined immunodeficiency (scid)/scid mice, in situ end labeling (ISEL)+ as well as CD80+ and CD86+ cell infiltrates appeared first in the blood vessel walls and pancreatic interstitial tissue at 2-3 weeks after transfer.
46	10206487	CD4+, CD8+, CD18+, CD44+, CD54+, and CD106+ cells then encircled and invaded some islets of the scid/scid mice 2 to 7 weeks after transfer.
47	10206487	Fas ligand was not present in Western blotting.
48	10206487	It is proposed that apoptosis commonly occurs in islet-infiltrating lymphocytes and that in the scid/scid adoptive-transfer model, the first islet-infiltrating cells are destroyed by programmed cell death independent of Fas ligand.
49	10206487	The role of CD8+ cells, cell degeneration, and Fas ligand in insulitis after intraperitoneal transfer of NOD splenocytes.
50	10206487	Cells expressing CD4, CD8, CD18, CD49d/CD29, CD44, CD54, CD80, CD86, CD106, CD11b/CD18 or DNA breaks were stained in the pancreases of female or male scid/ scid mice after adoptive transfer of lymphocytes from older than 12-week female nonobese diabetic (NOD) or Balb/c mice.
51	10206487	After intraperitoneal adoptive transfer of NOD splenocytes to female severe combined immunodeficiency (scid)/scid mice, in situ end labeling (ISEL)+ as well as CD80+ and CD86+ cell infiltrates appeared first in the blood vessel walls and pancreatic interstitial tissue at 2-3 weeks after transfer.
52	10206487	CD4+, CD8+, CD18+, CD44+, CD54+, and CD106+ cells then encircled and invaded some islets of the scid/scid mice 2 to 7 weeks after transfer.
53	10206487	Fas ligand was not present in Western blotting.
54	10206487	It is proposed that apoptosis commonly occurs in islet-infiltrating lymphocytes and that in the scid/scid adoptive-transfer model, the first islet-infiltrating cells are destroyed by programmed cell death independent of Fas ligand.
55	10475094	High glucose induces enhanced monocyte adhesion to valvular endothelial cells via a mechanism involving ICAM-1, VCAM-1 and CD18.
56	10475094	Together, the results indicate that high glucose induces enhanced monocyte adhesion to VEC via a mechanism involving in part an osmotic effect and mainly the cell adhesion molecules: ICAM-1, VCAM-1 and CD18.
57	10475094	High glucose induces enhanced monocyte adhesion to valvular endothelial cells via a mechanism involving ICAM-1, VCAM-1 and CD18.
58	10475094	Together, the results indicate that high glucose induces enhanced monocyte adhesion to VEC via a mechanism involving in part an osmotic effect and mainly the cell adhesion molecules: ICAM-1, VCAM-1 and CD18.
59	11141487	Moreover, the antibody-based neutralization of intercellular adhesion molecule-1 and CD18 is shown to prevent both leukocyte adhesion and retinal endothelial cell injury and death.
60	11487176	Our study showed that the state of leukocyte adhesiveness/aggregation is slightly increased in those who had concomitant diabetes but that there was no difference regarding the expression of CD11b/CD18 and CD62L antigens on the surface of the peripheral blood white blood cells.
61	11790870	VCAM-1 expression on endothelial cell and increased expression of CD11b CD18 on monocytes may facilitate monocyte emigration and can represent one of the initial steps of vascular alteration.
62	11821258	Intercellular adhesion molecule-1 (ICAM-1) and the leukocyte integrin CD18 are required for these processes.
63	11821258	Following one week of diabetes, neutrophil CD11a, CD11b, and CD18 expression was increased significantly, as were retinal ICAM-1 levels.
64	11821258	Animals were treated with aspirin, a cyclooxygenase 2 (COX-2) inhibitor (meloxicam), or a soluble tumor necrosis factor alpha (TNF-alpha) receptor/Fc construct (TNFR-Fc, etanercept).
65	11821258	High-dose aspirin also reduced the expression of CD11a, CD11b, and CD18, whereas meloxicam and etanercept did not.
66	11821258	Taken together, these data identify COX-2 and TNF-alpha as operative in the early signature pathologies of diabetic retinopathy, a newly recognized inflammatory disease.
67	11821258	Intercellular adhesion molecule-1 (ICAM-1) and the leukocyte integrin CD18 are required for these processes.
68	11821258	Following one week of diabetes, neutrophil CD11a, CD11b, and CD18 expression was increased significantly, as were retinal ICAM-1 levels.
69	11821258	Animals were treated with aspirin, a cyclooxygenase 2 (COX-2) inhibitor (meloxicam), or a soluble tumor necrosis factor alpha (TNF-alpha) receptor/Fc construct (TNFR-Fc, etanercept).
70	11821258	High-dose aspirin also reduced the expression of CD11a, CD11b, and CD18, whereas meloxicam and etanercept did not.
71	11821258	Taken together, these data identify COX-2 and TNF-alpha as operative in the early signature pathologies of diabetic retinopathy, a newly recognized inflammatory disease.
72	11821258	Intercellular adhesion molecule-1 (ICAM-1) and the leukocyte integrin CD18 are required for these processes.
73	11821258	Following one week of diabetes, neutrophil CD11a, CD11b, and CD18 expression was increased significantly, as were retinal ICAM-1 levels.
74	11821258	Animals were treated with aspirin, a cyclooxygenase 2 (COX-2) inhibitor (meloxicam), or a soluble tumor necrosis factor alpha (TNF-alpha) receptor/Fc construct (TNFR-Fc, etanercept).
75	11821258	High-dose aspirin also reduced the expression of CD11a, CD11b, and CD18, whereas meloxicam and etanercept did not.
76	11821258	Taken together, these data identify COX-2 and TNF-alpha as operative in the early signature pathologies of diabetic retinopathy, a newly recognized inflammatory disease.
77	11839570	Retinal vascular endothelial growth factor induces intercellular adhesion molecule-1 and endothelial nitric oxide synthase expression and initiates early diabetic retinal leukocyte adhesion in vivo.
78	11839570	Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes.
79	11839570	However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown.
80	11839570	Confirmed diabetic animals were treated with a highly specific VEGF-neutralizing Flt-Fc construct (VEGF TrapA(40)).
81	11839570	Retinal ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabetic controls (n = 5, P < 0.0001).
82	11839570	VEGF TrapA(40) also potently suppressed diabetic leukocyte adhesion in retinal arterioles (47%, n = 11, P < 0.0001), venules (36%, n = 11, P < 0.0005), and capillaries (36%, n = 11, P < 0.001).
83	11839570	The expression of endothelial nitric oxide synthase (eNOS), a downstream mediator of VEGF activity, was increased in diabetic retina, and was potently suppressed with VEGF TrapA(40) treatment (n = 8, P < 0.005).
84	11839570	Further, VEGF TrapA(40) reduced the diabetes-related nitric oxide increases in the retinae of diabetic animals.
85	11839570	Although neutrophil CD11a, CD11b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expression of these integrin adhesion molecules.
86	11839570	Taken together, these data demonstrate that VEGF induces retinal ICAM-1 and eNOS expression and initiates early diabetic retinal leukocyte adhesion in vivo.
87	11839570	Retinal vascular endothelial growth factor induces intercellular adhesion molecule-1 and endothelial nitric oxide synthase expression and initiates early diabetic retinal leukocyte adhesion in vivo.
88	11839570	Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes.
89	11839570	However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown.
90	11839570	Confirmed diabetic animals were treated with a highly specific VEGF-neutralizing Flt-Fc construct (VEGF TrapA(40)).
91	11839570	Retinal ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabetic controls (n = 5, P < 0.0001).
92	11839570	VEGF TrapA(40) also potently suppressed diabetic leukocyte adhesion in retinal arterioles (47%, n = 11, P < 0.0001), venules (36%, n = 11, P < 0.0005), and capillaries (36%, n = 11, P < 0.001).
93	11839570	The expression of endothelial nitric oxide synthase (eNOS), a downstream mediator of VEGF activity, was increased in diabetic retina, and was potently suppressed with VEGF TrapA(40) treatment (n = 8, P < 0.005).
94	11839570	Further, VEGF TrapA(40) reduced the diabetes-related nitric oxide increases in the retinae of diabetic animals.
95	11839570	Although neutrophil CD11a, CD11b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expression of these integrin adhesion molecules.
96	11839570	Taken together, these data demonstrate that VEGF induces retinal ICAM-1 and eNOS expression and initiates early diabetic retinal leukocyte adhesion in vivo.
97	11839570	Retinal vascular endothelial growth factor induces intercellular adhesion molecule-1 and endothelial nitric oxide synthase expression and initiates early diabetic retinal leukocyte adhesion in vivo.
98	11839570	Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes.
99	11839570	However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown.
100	11839570	Confirmed diabetic animals were treated with a highly specific VEGF-neutralizing Flt-Fc construct (VEGF TrapA(40)).
101	11839570	Retinal ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabetic controls (n = 5, P < 0.0001).
102	11839570	VEGF TrapA(40) also potently suppressed diabetic leukocyte adhesion in retinal arterioles (47%, n = 11, P < 0.0001), venules (36%, n = 11, P < 0.0005), and capillaries (36%, n = 11, P < 0.001).
103	11839570	The expression of endothelial nitric oxide synthase (eNOS), a downstream mediator of VEGF activity, was increased in diabetic retina, and was potently suppressed with VEGF TrapA(40) treatment (n = 8, P < 0.005).
104	11839570	Further, VEGF TrapA(40) reduced the diabetes-related nitric oxide increases in the retinae of diabetic animals.
105	11839570	Although neutrophil CD11a, CD11b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expression of these integrin adhesion molecules.
106	11839570	Taken together, these data demonstrate that VEGF induces retinal ICAM-1 and eNOS expression and initiates early diabetic retinal leukocyte adhesion in vivo.
107	12237478	The PMN adhesion molecules (CD11a, CD11b, CD11c, CD18) were evaluated using indirect immunofluorescence and a flow cytometer, at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-leucyl-phenyl-alanine (fMLP).
108	12237478	At baseline, in diabetic subjects the phenotypical expression of CD11a and CD11b was significantly reduced and CD11c was increased, whereas CD18 was unchanged in comparison with normals.
109	12237478	Considering type 1 and 2 diabetic subjects separately, CD11a was reduced and CD11c was increased in both subgroups, CD11b was decreased only in type 1 diabetics and CD18, decreased in type 1, was increased in type 2 subjects.
110	12237478	After activation with PMA and fMLP, in normal subjects we observed a significant increase of all PMN adhesion molecules whereas in diabetic subjects only CD11c increased significantly with both activating agents, and CD11b increased only after PMA activation.
111	12237478	In type 1 diabetic subjects only CD11c expression was increased, and in type 2 diabetic subjects an increase of CD11b (with PMA) and an increase of CD11c (with fMLP) were noted.
112	12237478	The PMN adhesion molecules (CD11a, CD11b, CD11c, CD18) were evaluated using indirect immunofluorescence and a flow cytometer, at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-leucyl-phenyl-alanine (fMLP).
113	12237478	At baseline, in diabetic subjects the phenotypical expression of CD11a and CD11b was significantly reduced and CD11c was increased, whereas CD18 was unchanged in comparison with normals.
114	12237478	Considering type 1 and 2 diabetic subjects separately, CD11a was reduced and CD11c was increased in both subgroups, CD11b was decreased only in type 1 diabetics and CD18, decreased in type 1, was increased in type 2 subjects.
115	12237478	After activation with PMA and fMLP, in normal subjects we observed a significant increase of all PMN adhesion molecules whereas in diabetic subjects only CD11c increased significantly with both activating agents, and CD11b increased only after PMA activation.
116	12237478	In type 1 diabetic subjects only CD11c expression was increased, and in type 2 diabetic subjects an increase of CD11b (with PMA) and an increase of CD11c (with fMLP) were noted.
117	12237478	The PMN adhesion molecules (CD11a, CD11b, CD11c, CD18) were evaluated using indirect immunofluorescence and a flow cytometer, at baseline and after in vitro activation with 4-phorbol 12-myristate 13-acetate (PMA) and N-formyl-methionyl-leucyl-phenyl-alanine (fMLP).
118	12237478	At baseline, in diabetic subjects the phenotypical expression of CD11a and CD11b was significantly reduced and CD11c was increased, whereas CD18 was unchanged in comparison with normals.
119	12237478	Considering type 1 and 2 diabetic subjects separately, CD11a was reduced and CD11c was increased in both subgroups, CD11b was decreased only in type 1 diabetics and CD18, decreased in type 1, was increased in type 2 subjects.
120	12237478	After activation with PMA and fMLP, in normal subjects we observed a significant increase of all PMN adhesion molecules whereas in diabetic subjects only CD11c increased significantly with both activating agents, and CD11b increased only after PMA activation.
121	12237478	In type 1 diabetic subjects only CD11c expression was increased, and in type 2 diabetic subjects an increase of CD11b (with PMA) and an increase of CD11c (with fMLP) were noted.
122	12682824	We evaluated the expression of some PMN integrins (CD11a, CD11b, CD11c, CD18), using flow cytofluorimetry, at baseline and after in vitro activation with 4-phorbol-12-myristate-13 acetate.
123	12682824	Type 2 diabetic subjects with MVC showed, compared to normals, an increase of CD11a and CD18 and a decrease of CD11b and CD11c.
124	12682824	After activation, in PMN(s) of normal subjects, we found an increase in the expression of all adhesion molecules, while in PMNS of type 2 diabetic subjects with MVC we observed an increase of CD11b and CD11c and a decrease of CD11a.
125	12682824	In type 2 diabetic patients with MVC the basal upregulation of CD11a and CD18 may be related to the PMN spontaneous activation, while the behavior of CD11b may depend on its self-consumption.
126	12682824	We evaluated the expression of some PMN integrins (CD11a, CD11b, CD11c, CD18), using flow cytofluorimetry, at baseline and after in vitro activation with 4-phorbol-12-myristate-13 acetate.
127	12682824	Type 2 diabetic subjects with MVC showed, compared to normals, an increase of CD11a and CD18 and a decrease of CD11b and CD11c.
128	12682824	After activation, in PMN(s) of normal subjects, we found an increase in the expression of all adhesion molecules, while in PMNS of type 2 diabetic subjects with MVC we observed an increase of CD11b and CD11c and a decrease of CD11a.
129	12682824	In type 2 diabetic patients with MVC the basal upregulation of CD11a and CD18 may be related to the PMN spontaneous activation, while the behavior of CD11b may depend on its self-consumption.
130	12682824	We evaluated the expression of some PMN integrins (CD11a, CD11b, CD11c, CD18), using flow cytofluorimetry, at baseline and after in vitro activation with 4-phorbol-12-myristate-13 acetate.
131	12682824	Type 2 diabetic subjects with MVC showed, compared to normals, an increase of CD11a and CD18 and a decrease of CD11b and CD11c.
132	12682824	After activation, in PMN(s) of normal subjects, we found an increase in the expression of all adhesion molecules, while in PMNS of type 2 diabetic subjects with MVC we observed an increase of CD11b and CD11c and a decrease of CD11a.
133	12682824	In type 2 diabetic patients with MVC the basal upregulation of CD11a and CD18 may be related to the PMN spontaneous activation, while the behavior of CD11b may depend on its self-consumption.
134	12872395	[Effect of Chinese herbal medicine for activating blood circulation to remove stasis on CD11b/CD18 expression in patients with diabetes mellitus type 2].
135	12906027	The pre- and postprocedural plasma levels of IL-8 and serum C-reactive protein (CRP) were examined by immunoassay, and the expression of CD11b/CD18 on neutrophils was assessed by flow cytometry.
136	12906027	Sixteen patients with early complications had high preprocedural levels and high postprocedural differentials of IL-8, CRP, and CD11b/CD18 compared to those without complications (all P < 0.05).
137	12906027	The occurrence of complications showed a significant increase in the patients according to the tertiles of IL-8, CRP, and CD11b/CD18.
138	12906027	There were significant correlations in the postprocedural differential between IL-8 and CD11b/CD18 (r = 0.776, P = 0.002) in patients with complications.
139	12906027	The pre- and postprocedural plasma levels of IL-8 and serum C-reactive protein (CRP) were examined by immunoassay, and the expression of CD11b/CD18 on neutrophils was assessed by flow cytometry.
140	12906027	Sixteen patients with early complications had high preprocedural levels and high postprocedural differentials of IL-8, CRP, and CD11b/CD18 compared to those without complications (all P < 0.05).
141	12906027	The occurrence of complications showed a significant increase in the patients according to the tertiles of IL-8, CRP, and CD11b/CD18.
142	12906027	There were significant correlations in the postprocedural differential between IL-8 and CD11b/CD18 (r = 0.776, P = 0.002) in patients with complications.
143	12906027	The pre- and postprocedural plasma levels of IL-8 and serum C-reactive protein (CRP) were examined by immunoassay, and the expression of CD11b/CD18 on neutrophils was assessed by flow cytometry.
144	12906027	Sixteen patients with early complications had high preprocedural levels and high postprocedural differentials of IL-8, CRP, and CD11b/CD18 compared to those without complications (all P < 0.05).
145	12906027	The occurrence of complications showed a significant increase in the patients according to the tertiles of IL-8, CRP, and CD11b/CD18.
146	12906027	There were significant correlations in the postprocedural differential between IL-8 and CD11b/CD18 (r = 0.776, P = 0.002) in patients with complications.
147	12906027	The pre- and postprocedural plasma levels of IL-8 and serum C-reactive protein (CRP) were examined by immunoassay, and the expression of CD11b/CD18 on neutrophils was assessed by flow cytometry.
148	12906027	Sixteen patients with early complications had high preprocedural levels and high postprocedural differentials of IL-8, CRP, and CD11b/CD18 compared to those without complications (all P < 0.05).
149	12906027	The occurrence of complications showed a significant increase in the patients according to the tertiles of IL-8, CRP, and CD11b/CD18.
150	12906027	There were significant correlations in the postprocedural differential between IL-8 and CD11b/CD18 (r = 0.776, P = 0.002) in patients with complications.
151	14623906	In vitro, RAGE-dependent leukocyte adhesion to endothelial cells was mediated by a direct interaction of RAGE with the beta2-integrin Mac-1 and, to a lower extent, with p150,95 but not with LFA-1 or with beta1-integrins.
152	14623906	The RAGE-Mac-1 interaction was augmented by the proinflammatory RAGE-ligand, S100-protein.
153	15111316	The expression of intercellular adhesion molecule-1 (ICAM-1) and the CD18 (the common beta-chain of ICAM-1 ligands) were both suppressed with simvastatin.
154	15111316	This suggests that simvastatin attenuates leukocyte-endothelial cell interactions and subsequent blood-retinal barrier breakdown via suppression of vascular endothelial growth factor-induced ICAM-1 expression in the diabetic retina.
155	15231732	Retinal leukostasis increases within days of developing diabetes and correlates with the increased expression of retinal intercellular adhesion molecule-1 (ICAM-1) and CD18.
156	15231732	Mice deficient in the genes encoding for the leukocyte adhesion molecules CD18 and ICAM-1 were studied in two models of diabetic retinopathy with respect to the long-term development of retinal vascular lesions.
157	15231732	These changes are significantly reduced in CD18- and ICAM-1-deficient mice.
158	15231732	Retinal leukostasis increases within days of developing diabetes and correlates with the increased expression of retinal intercellular adhesion molecule-1 (ICAM-1) and CD18.
159	15231732	Mice deficient in the genes encoding for the leukocyte adhesion molecules CD18 and ICAM-1 were studied in two models of diabetic retinopathy with respect to the long-term development of retinal vascular lesions.
160	15231732	These changes are significantly reduced in CD18- and ICAM-1-deficient mice.
161	15231732	Retinal leukostasis increases within days of developing diabetes and correlates with the increased expression of retinal intercellular adhesion molecule-1 (ICAM-1) and CD18.
162	15231732	Mice deficient in the genes encoding for the leukocyte adhesion molecules CD18 and ICAM-1 were studied in two models of diabetic retinopathy with respect to the long-term development of retinal vascular lesions.
163	15231732	These changes are significantly reduced in CD18- and ICAM-1-deficient mice.
164	15277376	Increased serum levels of MRP-8/14 in type 1 diabetes induce an increased expression of CD11b and an enhanced adhesion of circulating monocytes to fibronectin.
165	15277376	Monocytes of type 1 diabetic patients displayed an increased adhesion to fibronectin in comparison with type 2 patients and healthy control subjects but had a normal expression of the FN binding integrins CD29, CD49a, CD49d, and CD49e (although CD11b and CD18 expression was increased).
166	15277376	MRP-8/14, which was increased in the sera of type 1 diabetic patients, induced healthy donor monocytes to adhere to FN and upregulate CD11b expression in a dosage-dependent manner.
167	15558232	Monocytic expression of CD14 and CD18, circulating adhesion molecules and inflammatory markers in women with diabetes mellitus and impaired glucose tolerance.
168	16129698	Six weeks after STZ injection, impairment of left ventricular (LV) function parameters measured by a Millar-tip catheter (peak LV systolic pressure; dP/dtmax; dP/dtmin) was accompanied by a significant increment of ICAM-1 and VCAM-1 (CAMs) expression, as well as of beta2-leukocyte-integrins+ (CD18+, CD11a+, CD11b+) and cytokine (TNF-alpha and IL-1beta)-expressing infiltrates in male Sprague-Dawley (SD-STZ) rats compared with normoglycemic littermates.
169	16235772	Hemoglobin, high sensitive C-reactive protein (hsCRP), creatinine, blood lipids, white blood cells (WBC); CD11b/CD18; vascular cell adhesion molecule (sVCAM-1), intercellular adhesion molecule (sICAM-1), sE-selectin, sP-selectin; IL-6, IL-8, tumour necrosis factor (TNF)alpha, sTNFalpha-R1 and sTNFalpha-R2 were analysed.
170	17166396	We examined the expression of genes encoding the cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and transforming growth factor-beta1 (TGF-beta1) as well as the pan-leukocyte marker CD18.
171	17166396	TNF-alpha (P<0.05) and TGF-beta1 transcripts (P<0.05) increased over time in the EX group, but these increases did not differ from those in the CON group.
172	17349081	Lymphocyte CD11a/CD18 expressions were higher at 6 h, whereas the percentage was lower at 24 h in the SO group than in the FO group.
173	17349081	Neutrophil CD11b/CD18 expressions were significantly higher in the SO group than in the FO group at 0 h.
174	17349081	Lymphocyte CD11a/CD18 expressions were higher at 6 h, whereas the percentage was lower at 24 h in the SO group than in the FO group.
175	17349081	Neutrophil CD11b/CD18 expressions were significantly higher in the SO group than in the FO group at 0 h.
176	17477023	This led us to examine TGF-beta1 regulation when the effects of macrophage derived cytokines such as platelet derived growth factor and interleukin-1 are combined with exposure to elevated glucose concentrations.
177	17477023	In addition, direct interaction between monocyte-macrophage CD18 and PTC cell surface ICAM-1 stimulates TGF-beta1 synthesis.
178	17477023	We have now identified HA based structures synthesised on the surface of PTC, which act to prevent PTC-macrophage interaction through ICAM-1 thus preventing macrophage driven TGF-beta1 synthesis.
179	17549301	Biphasic effect of pioglitazone on isolated human endothelial progenitor cells: involvement of peroxisome proliferator-activated receptor-gamma and transforming growth factor-beta1.
180	17549301	We evaluated the effects of the anti-diabetic drug pioglitazone on human EPC function and the involvement of PPAR-gamma and TGF-beta1.
181	17549301	EPCs in culture were characterized at day 7 by the development of colony-forming units (CFUs) and flow cytometry assessment of differentiation marker (DiI-ac-LDL/lectin, KDR and CD31).
182	17549301	Treatment with pioglitazone for 72 hours increased the number of EPC-CFUs, DiI-ac-LDL(+)/lectin(+), CD31(+) and KDR(+) EPCs at 1 microM but not at 10 microM.
183	17549301	Indeed, pioglitazone increased EPC adhesion in flow at 1 microM, an effect prevented by PPAR-gamma and beta2-integrin blockade.
184	17549301	As determined by ELISA, pioglitazone induced a persistent increase in TGF-beta1 secretion only at 10 microM when a significantly elevated expression of endoglin, the accessory receptor for TGF-beta1, was also observed.
185	17909696	Intercellular adhesion molecule (ICAM)-1, vascular adhesion molecule (VCAM)-1, beta2-lymphocyte-integrins(+) (CD18(+), CD11a(+), CD11b(+)), ED1/CD68(+) and cytokine (TNF-alpha, interleukin (IL)-1beta)- expressing infiltrates, total collagen content and stainings of collagen I and III were quantified by digital image analysis.
186	17909696	TNFalpha-antagonism reduced ICAM-1- and VCAM-1 expression and leukocyte infiltration to levels of non-diabetics and decreased macrophage residence by 3.3-fold compared with untreated diabetics.
187	17909696	In addition, anti-TNF-alpha mAb-treatment decreased diabetes-induced cardiac TNF-alpha and IL-1beta expression by 2.0-fold and 1.8- fold, respectively, and reduced the ratio of phosphorylated to total ERK by 2.7-fold.
188	17909696	The reduction in intramyocardial inflammation was associated with a 5.4-fold and 3.6-fold reduction in cardiac collagen I and III content, respectively.
189	17927013	Insulin/glucose-insulin-potassium (GIK) regimen suppresses the production of tumor necrosis factor-alpha (TNF-alpha), interleukins-6 (IL-6), macrophage migration inhibitory factor (MIF) and other pro-inflammatory cytokines and reactive oxygen species (ROS), enhances the synthesis of endothelial nitric oxide (eNO), and anti-inflammatory cytokines interleukins-4 (IL-4) and interleukin-10 (IL-10).
190	17927013	In subjects who are critically ill, monocyte HLA-DR expression was significantly decreased with a concomitant increase in plasma IL-10 and IL-4 concentrations.
191	17927013	Large increases in the plasma concentrations of TNF-alpha, IL-6, sustained increase in the expression of leukocyte CD11b/CD18, and ROS generation following surgery and infections were found to be associated with increased mortality.
192	19073595	The heparan sulfate proteoglycan form of epithelial CD44v3 serves as a CD11b/CD18 counter-receptor during polymorphonuclear leukocyte transepithelial migration.
193	19073595	Leukocyte beta2-integrin CD11b/CD18 mediates the firm adhesion and subsequent transepithelial migration of polymorphonuclear leukocytes, but the identity of its counter-receptor(s) on epithelia remains elusive.
194	19073595	Here we identified a monoclonal antibody, clone C3H7, which strongly bound to the basolateral membranes of epithelial cells and inhibited both the adhesion of epithelial cells to immobilized CD11b/CD8 and the transepithelial migration of PMNs in a physiologically relevant basolateral-to-apical direction.
195	19073595	C3H7 antigen expression in epithelial monolayers was significantly increased by treatment with proinflammatory cytokine interferon-gamma or a combination of interferon-gamma and tumor necrosis factor-alpha.
196	19073595	Further studies demonstrated that this epithelial CD44v3 specifically binds to CD11b/CD18 through its heparan sulfate moieties.
197	19073595	In summary, our study demonstrates for the first time that the heparan sulfate proteoglycan form of epithelial CD44v3 plays a critical role in facilitating PMN recruitment during inflammatory episodes via directly binding to CD11b/CD18.
198	19073595	The heparan sulfate proteoglycan form of epithelial CD44v3 serves as a CD11b/CD18 counter-receptor during polymorphonuclear leukocyte transepithelial migration.
199	19073595	Leukocyte beta2-integrin CD11b/CD18 mediates the firm adhesion and subsequent transepithelial migration of polymorphonuclear leukocytes, but the identity of its counter-receptor(s) on epithelia remains elusive.
200	19073595	Here we identified a monoclonal antibody, clone C3H7, which strongly bound to the basolateral membranes of epithelial cells and inhibited both the adhesion of epithelial cells to immobilized CD11b/CD8 and the transepithelial migration of PMNs in a physiologically relevant basolateral-to-apical direction.
201	19073595	C3H7 antigen expression in epithelial monolayers was significantly increased by treatment with proinflammatory cytokine interferon-gamma or a combination of interferon-gamma and tumor necrosis factor-alpha.
202	19073595	Further studies demonstrated that this epithelial CD44v3 specifically binds to CD11b/CD18 through its heparan sulfate moieties.
203	19073595	In summary, our study demonstrates for the first time that the heparan sulfate proteoglycan form of epithelial CD44v3 plays a critical role in facilitating PMN recruitment during inflammatory episodes via directly binding to CD11b/CD18.
204	19073595	The heparan sulfate proteoglycan form of epithelial CD44v3 serves as a CD11b/CD18 counter-receptor during polymorphonuclear leukocyte transepithelial migration.
205	19073595	Leukocyte beta2-integrin CD11b/CD18 mediates the firm adhesion and subsequent transepithelial migration of polymorphonuclear leukocytes, but the identity of its counter-receptor(s) on epithelia remains elusive.
206	19073595	Here we identified a monoclonal antibody, clone C3H7, which strongly bound to the basolateral membranes of epithelial cells and inhibited both the adhesion of epithelial cells to immobilized CD11b/CD8 and the transepithelial migration of PMNs in a physiologically relevant basolateral-to-apical direction.
207	19073595	C3H7 antigen expression in epithelial monolayers was significantly increased by treatment with proinflammatory cytokine interferon-gamma or a combination of interferon-gamma and tumor necrosis factor-alpha.
208	19073595	Further studies demonstrated that this epithelial CD44v3 specifically binds to CD11b/CD18 through its heparan sulfate moieties.
209	19073595	In summary, our study demonstrates for the first time that the heparan sulfate proteoglycan form of epithelial CD44v3 plays a critical role in facilitating PMN recruitment during inflammatory episodes via directly binding to CD11b/CD18.
210	19073595	The heparan sulfate proteoglycan form of epithelial CD44v3 serves as a CD11b/CD18 counter-receptor during polymorphonuclear leukocyte transepithelial migration.
211	19073595	Leukocyte beta2-integrin CD11b/CD18 mediates the firm adhesion and subsequent transepithelial migration of polymorphonuclear leukocytes, but the identity of its counter-receptor(s) on epithelia remains elusive.
212	19073595	Here we identified a monoclonal antibody, clone C3H7, which strongly bound to the basolateral membranes of epithelial cells and inhibited both the adhesion of epithelial cells to immobilized CD11b/CD8 and the transepithelial migration of PMNs in a physiologically relevant basolateral-to-apical direction.
213	19073595	C3H7 antigen expression in epithelial monolayers was significantly increased by treatment with proinflammatory cytokine interferon-gamma or a combination of interferon-gamma and tumor necrosis factor-alpha.
214	19073595	Further studies demonstrated that this epithelial CD44v3 specifically binds to CD11b/CD18 through its heparan sulfate moieties.
215	19073595	In summary, our study demonstrates for the first time that the heparan sulfate proteoglycan form of epithelial CD44v3 plays a critical role in facilitating PMN recruitment during inflammatory episodes via directly binding to CD11b/CD18.
216	19223596	Genetic deficiency of Itgb2 or ItgaL prevents autoimmune diabetes through distinctly different mechanisms in NOD/LtJ mice.
217	19353220	We prospectively examined serial changes in p-selectin glycoprotein ligand-1 (PSGL-1), macrophage antigen-1 (Mac-1), and lymphocyte function-associated antigen-1 (LFA-1) expression by leukocyte subsets using flow cytometry at various time points in 65 acute ischemic stroke patients and 60 controls.
218	19353220	The expression of monocyte Mac-1, LFA-1, and neutrophil Mac-1 were also significantly increased on days 1 and 7 after stroke than in control subjects (p < 0.05).
219	19353220	This study shows that higher neutrophil PSGL-1 expression on admission may imply a higher risk for END and that monocyte Mac-1 expression on admission reflects the severity of ischemic stroke on admission.
220	19353220	We prospectively examined serial changes in p-selectin glycoprotein ligand-1 (PSGL-1), macrophage antigen-1 (Mac-1), and lymphocyte function-associated antigen-1 (LFA-1) expression by leukocyte subsets using flow cytometry at various time points in 65 acute ischemic stroke patients and 60 controls.
221	19353220	The expression of monocyte Mac-1, LFA-1, and neutrophil Mac-1 were also significantly increased on days 1 and 7 after stroke than in control subjects (p < 0.05).
222	19353220	This study shows that higher neutrophil PSGL-1 expression on admission may imply a higher risk for END and that monocyte Mac-1 expression on admission reflects the severity of ischemic stroke on admission.
223	19353220	We prospectively examined serial changes in p-selectin glycoprotein ligand-1 (PSGL-1), macrophage antigen-1 (Mac-1), and lymphocyte function-associated antigen-1 (LFA-1) expression by leukocyte subsets using flow cytometry at various time points in 65 acute ischemic stroke patients and 60 controls.
224	19353220	The expression of monocyte Mac-1, LFA-1, and neutrophil Mac-1 were also significantly increased on days 1 and 7 after stroke than in control subjects (p < 0.05).
225	19353220	This study shows that higher neutrophil PSGL-1 expression on admission may imply a higher risk for END and that monocyte Mac-1 expression on admission reflects the severity of ischemic stroke on admission.
226	20928981	In addition to advanced glycation end products (AGE), RAGE has other important ligands such as: high mobility group box 1 protein (HMGB1, also termed amphoterin), the group of calcium binding cellular factors S100 (also termed calgranulin), amiloid beta peptides and Mac-1, a beta-2 integrin (CD1lb/CD18).