Ignet

Gene Information

Gene symbol: TDGF3

Gene name: teratocarcinoma-derived growth factor 3, pseudogene

HGNC ID: 11703

Related Genes

#	Gene Symbol	Number of hits
1	ADCY10	1 hits
2	CASP8	1 hits
3	CD79A	1 hits
4	CD8A	1 hits
5	CLEC7A	1 hits
6	CR1	1 hits
7	CR2	1 hits
8	FCAR	1 hits
9	IFN1	1 hits
10	IFNG	1 hits
11	IL1B	1 hits
12	IL6	1 hits
13	ITGAM	1 hits
14	ITGAX	1 hits
15	ITGB2	1 hits
16	NLRP3	1 hits
17	TDGF4	1 hits
18	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	1460286	By analytic flow cytometry, the mice immunized with PRP-OMPC demonstrated an increase in large splenocytes expressing the Ag Mac-1 (CD11b, CR3).
2	1460286	By immunohistochemical staining, the cells were identified as macrophages due to expression of Mac-1 and p150,95 (CD11C) Ag.
3	1460286	After PRP-OMPC immunization, severe combined immunodeficient mice also demonstrated significant splenomegaly with an increase in macrophages identified by expression of Mac-1 and MHC class II Ag.
4	10408367	These iC3b fragments serve to promote the high avidity attachment of the 'iC3b-opsonized' pathogens to the iC3b-receptors (CR3, CD11b/CD18) of phagocytic cells and natural killer (NK) cells, stimulating phagocytosis and/or cytotoxic degranulation.
5	10408367	Moreover, the cytotoxic activation of beta-glucan-primed NK cell CR3 by iC3b-opsonized tumors is shown to be accompanied by a tumor-localized secretion of the cytokines TNFalpha, IFNalpha, IFNgamma, and IL-6.
6	10408367	These iC3b fragments serve to promote the high avidity attachment of the 'iC3b-opsonized' pathogens to the iC3b-receptors (CR3, CD11b/CD18) of phagocytic cells and natural killer (NK) cells, stimulating phagocytosis and/or cytotoxic degranulation.
7	10408367	Moreover, the cytotoxic activation of beta-glucan-primed NK cell CR3 by iC3b-opsonized tumors is shown to be accompanied by a tumor-localized secretion of the cytokines TNFalpha, IFNalpha, IFNgamma, and IL-6.
8	10525053	Both S. pneumoniae-bound IgA and complement were involved, as demonstrated by a 50% decrease in killing with blocking of Fcalpha receptor (CD89) and CR1/CR3 (CD35/CD11b).
9	10525053	However, IgA-mediated killing by phagocytes could be reproduced in the absence of opsonic complement by pre-activating phagocytes with the inflammatory products C5a and TNF-alpha.
10	11075934	We have previously demonstrated that the alphaMbeta2 integrin (known as CR3 or Mac-1) expressed on neutrophils (PMNs) and/or on CHO Mac-1 transfected cells,in the presence of serum complement binds B. burgdorferi and promotes an increased non -opsonic adhesion, in the presence of serum complement.
11	12549976	Complement receptor 3 (CR3; CD18/CD11b) plays an important role in the recognition and clearance of Streptococcus pneumoniae (pneumococci) by neutrophils.
12	14615141	The HIV-1 chimeric protein CR3 expressed by poxviral vectors induces a diverse CD8+ T cell response in mice and is antigenic for PBMCs from HIV+ patients.
13	14615141	Mice immunised twice intraperitoneally with FPCR3, developed a CD8(+) T cell response measured as production of IFN-gamma by splenocytes in response to stimulation with P815 cells infected with recombinant vaccinia viruses (rVV) expressing CR3, Gag and Nef.
14	14615141	The number of IFN-gamma secreting cells was markedly higher when a P815 cell line constitutively expressing CR3 was used as target cells for Enzyme-linked-immunospot (ELISPOT).
15	14615141	The HIV-1 chimeric protein CR3 expressed by poxviral vectors induces a diverse CD8+ T cell response in mice and is antigenic for PBMCs from HIV+ patients.
16	14615141	Mice immunised twice intraperitoneally with FPCR3, developed a CD8(+) T cell response measured as production of IFN-gamma by splenocytes in response to stimulation with P815 cells infected with recombinant vaccinia viruses (rVV) expressing CR3, Gag and Nef.
17	14615141	The number of IFN-gamma secreting cells was markedly higher when a P815 cell line constitutively expressing CR3 was used as target cells for Enzyme-linked-immunospot (ELISPOT).
18	14615141	The HIV-1 chimeric protein CR3 expressed by poxviral vectors induces a diverse CD8+ T cell response in mice and is antigenic for PBMCs from HIV+ patients.
19	14615141	Mice immunised twice intraperitoneally with FPCR3, developed a CD8(+) T cell response measured as production of IFN-gamma by splenocytes in response to stimulation with P815 cells infected with recombinant vaccinia viruses (rVV) expressing CR3, Gag and Nef.
20	14615141	The number of IFN-gamma secreting cells was markedly higher when a P815 cell line constitutively expressing CR3 was used as target cells for Enzyme-linked-immunospot (ELISPOT).
21	15926077	The Bordetella adenylate cyclase toxoid (CyaA) targets cells expressing the alphaMbeta2 integrin receptor CD11b/CD18 (CR3 or Mac-1) and can penetrate into cytosol of professional antigen-presenting cells, such as dendritic cells.
22	15926077	We show here that vaccination with a genetically detoxified CyaA336/E7 protein, carrying the full-length oncoprotein E7 of the human papilloma virus 16 inserted at position 336 of the cell-invasive AC domain of CyaA, induces an E7-specific CD8+ T-cell immune response and confers on mice protective, as well as therapeutic immunity against challenge with TC-1 tumor cells expressing the E7 oncoprotein.
23	16675078	The major toxic effects of native CyaA are attributed to its enzymatic activity following delivery to cells of the innate immune system via the CD11b/CD18 (CR3) cell receptor.
24	16675078	In view of the potential use of detoxified CyaA in vaccinology, a complement dependent in vitro model was used to investigate the potential effects of the interaction of detoxified CyaA with CD11b/CD18 (CR3) on phagocytic function.
25	16675078	Interaction of CyaA with CD11b/CD18 (CR3) on human pro-myelocytic NB-4 cells differentiated to a neutrophil-like phenotype was measured as inhibition of binding of a monoclonal antibody to the receptor.
26	16675078	However, availability of CD11b/CD18 receptors on acylated CyaA-treated cells was restored after washing and further incubation.
27	16675078	The results suggest that the interaction of detoxified CyaA constructs to the CD11b/CD18 (CR3) receptor may temporarily influence the complement-dependent phagocytic function in neutrophil leukocytes.
28	16675078	The major toxic effects of native CyaA are attributed to its enzymatic activity following delivery to cells of the innate immune system via the CD11b/CD18 (CR3) cell receptor.
29	16675078	In view of the potential use of detoxified CyaA in vaccinology, a complement dependent in vitro model was used to investigate the potential effects of the interaction of detoxified CyaA with CD11b/CD18 (CR3) on phagocytic function.
30	16675078	Interaction of CyaA with CD11b/CD18 (CR3) on human pro-myelocytic NB-4 cells differentiated to a neutrophil-like phenotype was measured as inhibition of binding of a monoclonal antibody to the receptor.
31	16675078	However, availability of CD11b/CD18 receptors on acylated CyaA-treated cells was restored after washing and further incubation.
32	16675078	The results suggest that the interaction of detoxified CyaA constructs to the CD11b/CD18 (CR3) receptor may temporarily influence the complement-dependent phagocytic function in neutrophil leukocytes.
33	16675078	The major toxic effects of native CyaA are attributed to its enzymatic activity following delivery to cells of the innate immune system via the CD11b/CD18 (CR3) cell receptor.
34	16675078	In view of the potential use of detoxified CyaA in vaccinology, a complement dependent in vitro model was used to investigate the potential effects of the interaction of detoxified CyaA with CD11b/CD18 (CR3) on phagocytic function.
35	16675078	Interaction of CyaA with CD11b/CD18 (CR3) on human pro-myelocytic NB-4 cells differentiated to a neutrophil-like phenotype was measured as inhibition of binding of a monoclonal antibody to the receptor.
36	16675078	However, availability of CD11b/CD18 receptors on acylated CyaA-treated cells was restored after washing and further incubation.
37	16675078	The results suggest that the interaction of detoxified CyaA constructs to the CD11b/CD18 (CR3) receptor may temporarily influence the complement-dependent phagocytic function in neutrophil leukocytes.
38	16675078	The major toxic effects of native CyaA are attributed to its enzymatic activity following delivery to cells of the innate immune system via the CD11b/CD18 (CR3) cell receptor.
39	16675078	In view of the potential use of detoxified CyaA in vaccinology, a complement dependent in vitro model was used to investigate the potential effects of the interaction of detoxified CyaA with CD11b/CD18 (CR3) on phagocytic function.
40	16675078	Interaction of CyaA with CD11b/CD18 (CR3) on human pro-myelocytic NB-4 cells differentiated to a neutrophil-like phenotype was measured as inhibition of binding of a monoclonal antibody to the receptor.
41	16675078	However, availability of CD11b/CD18 receptors on acylated CyaA-treated cells was restored after washing and further incubation.
42	16675078	The results suggest that the interaction of detoxified CyaA constructs to the CD11b/CD18 (CR3) receptor may temporarily influence the complement-dependent phagocytic function in neutrophil leukocytes.
43	16682479	Preincubation with TNF-alpha promoted CR3 expression on BMPMN, and this level of expression was also enhanced by WKYMVm.
44	16857732	Critical role for serum opsonins and complement receptors CR3 (CD11b/CD18) and CR4 (CD11c/CD18) in phagocytosis of Francisella tularensis by human dendritic cells (DC): uptake of Francisella leads to activation of immature DC and intracellular survival of the bacteria.
45	16857732	We demonstrate that complement factor C3-derived opsonins and the major complement receptors expressed by DC, the integrins CR3 (CD11b/CD18) and CR4 (CD11c/CD18), play a critical role in this adhesion-mediated phagocytosis.
46	16857732	LVS induced proinflammatory cytokine production and up-regulation of costimulatory surface proteins (CD40, CD86, and MHC Class II) on DC but resisted killing.
47	16857732	Serum-treated LVS rapidly induced (within 6 h) a number of cytokines including IL-10, a potent suppressor of macrophage functions and down-regulator of Th1-like responses and the Th1 response inducer IL-12.
48	16857732	These results suggest that the simultaneous production of an activating (IL-12, IL-1beta, and TNF-alpha) and a suppressing (IL-10) cytokine profile could contribute to the immunopathogenesis of tularemia.
49	16857732	Critical role for serum opsonins and complement receptors CR3 (CD11b/CD18) and CR4 (CD11c/CD18) in phagocytosis of Francisella tularensis by human dendritic cells (DC): uptake of Francisella leads to activation of immature DC and intracellular survival of the bacteria.
50	16857732	We demonstrate that complement factor C3-derived opsonins and the major complement receptors expressed by DC, the integrins CR3 (CD11b/CD18) and CR4 (CD11c/CD18), play a critical role in this adhesion-mediated phagocytosis.
51	16857732	LVS induced proinflammatory cytokine production and up-regulation of costimulatory surface proteins (CD40, CD86, and MHC Class II) on DC but resisted killing.
52	16857732	Serum-treated LVS rapidly induced (within 6 h) a number of cytokines including IL-10, a potent suppressor of macrophage functions and down-regulator of Th1-like responses and the Th1 response inducer IL-12.
53	16857732	These results suggest that the simultaneous production of an activating (IL-12, IL-1beta, and TNF-alpha) and a suppressing (IL-10) cytokine profile could contribute to the immunopathogenesis of tularemia.
54	17201666	We also studied several ways to mix the antigens and the impact on CR3-specific interferon (IFN)-gamma secretion.
55	17201666	In addition, CR3-specific IFN-gamma secretion of the various formulations tested was the same irrespective of the order in which the antigens were combined.
56	17201666	We also studied several ways to mix the antigens and the impact on CR3-specific interferon (IFN)-gamma secretion.
57	17201666	In addition, CR3-specific IFN-gamma secretion of the various formulations tested was the same irrespective of the order in which the antigens were combined.
58	17522213	Manipulation of sequence order, orientation, and composition of the CR2 and CR3 subdomains suggests that specific peptide sequences rather than RNA structures are responsible for synthesis retardation.
59	18855656	Currently, most of the vaccine candidates in clinical trials were developed to stimulate HIV-1-specific CD8+ cytotoxic (CTL) and CD4+ T helper (Th) lymphocytes.
60	18855656	According to our studies in mice, the nasal-subcutaneous co-administration of this multiantigenic formulation induces a strong Th1-biased specific response against CR3, CD8+ T cells in mice spleen and IFN-gamma-secreting cells in mesenteric lymph nodes.
61	18855656	Cross-reactive p24-specific IFN-gamma-secreting cells in spleen were also detected.
62	19003299	Taguchi's methods were used for the design of an experimental strategy aimed at optimizing cell density and monoclonal antibody (mAb) production from a spinner flask hybridoma culture. 23G11 is an antibody to the human leukocyte adhesion molecule, CR3 or beta 2 integrin (CD11b/CD18).
63	19018015	The Candida antigen CR3-RP (complement receptor 3-related protein) is supposed to be a 'mimicry' protein because of its ability to bind antibody directed against the alpha subunit of the mammalian CR3 (CD11b/CD18).
64	22888138	Finally, we demonstrate using receptor-blocking Abs that CR1 (CD35) and CR3 (CD11b/CD18) acted in concert for phagocytosis of opsonized F. tularensis by human neutrophils, whereas CR3 and CR4 (CD11c/CD18) mediated infection of human monocyte-derived macrophages.
65	22888138	Altogether, our data provide fundamental insight into mechanisms of F. tularensis phagocytosis and support a model whereby natural IgM binds to surface capsular and O-Ag polysaccharides of F. tularensis and initiates the classical complement cascade via C1q to promote C3 opsonization of the bacterium and phagocytosis via CR3 and either CR1 or CR4 in a phagocyte-specific manner.
66	25063877	Caspase-8 modulates dectin-1 and complement receptor 3-driven IL-1β production in response to β-glucans and the fungal pathogen, Candida albicans.
67	25063877	The nucleotide-binding domain and leucine-rich repeat containing family (NLR), pyrin domain-containing 3 (NLRP3) inflammasome plays a key role in triggering caspase-1-dependent IL-1β maturation and resistance to fungal dissemination in Candida albicans infection. β-Glucans are major components of fungal cell walls that trigger IL-1β secretion in both murine and human immune cells.
68	25063877	We show that the NLRP3-apoptosis-associated speck-like protein containing caspase recruitment domain protein-caspase-1 inflammasome is absolutely critical for IL-1β production in response to β-glucans.
69	25063877	Interestingly, we also found that both complement receptor 3 (CR3) and dectin-1 play a crucial role in coordinating β-glucan-induced IL-1β processing as well as a cell death response.
70	25063877	In addition to the essential role of caspase-1, we identify an important role for the proapoptotic protease caspase-8 in promoting β-glucan-induced cell death and NLRP3 inflammasome-dependent IL-1β maturation.
71	25063877	A strong requirement for CR3 and caspase-8 also was found for NLRP3-dependent IL-1β production in response to heat-killed C. albicans.
72	25063877	Taken together, these results define the importance of dectin-1, CR3, and caspase-8, in addition to the canonical NLRP3 inflammasome, in mediating β-glucan- and C. albicans-induced innate responses in dendritic cells.
73	25063877	Collectively, these findings establish a novel link between β-glucan recognition receptors and the inflammatory proteases caspase-8 and caspase-1 in coordinating cytokine secretion and cell death in response to immunostimulatory fungal components.
74	25063877	Caspase-8 modulates dectin-1 and complement receptor 3-driven IL-1β production in response to β-glucans and the fungal pathogen, Candida albicans.
75	25063877	The nucleotide-binding domain and leucine-rich repeat containing family (NLR), pyrin domain-containing 3 (NLRP3) inflammasome plays a key role in triggering caspase-1-dependent IL-1β maturation and resistance to fungal dissemination in Candida albicans infection. β-Glucans are major components of fungal cell walls that trigger IL-1β secretion in both murine and human immune cells.
76	25063877	We show that the NLRP3-apoptosis-associated speck-like protein containing caspase recruitment domain protein-caspase-1 inflammasome is absolutely critical for IL-1β production in response to β-glucans.
77	25063877	Interestingly, we also found that both complement receptor 3 (CR3) and dectin-1 play a crucial role in coordinating β-glucan-induced IL-1β processing as well as a cell death response.
78	25063877	In addition to the essential role of caspase-1, we identify an important role for the proapoptotic protease caspase-8 in promoting β-glucan-induced cell death and NLRP3 inflammasome-dependent IL-1β maturation.
79	25063877	A strong requirement for CR3 and caspase-8 also was found for NLRP3-dependent IL-1β production in response to heat-killed C. albicans.
80	25063877	Taken together, these results define the importance of dectin-1, CR3, and caspase-8, in addition to the canonical NLRP3 inflammasome, in mediating β-glucan- and C. albicans-induced innate responses in dendritic cells.
81	25063877	Collectively, these findings establish a novel link between β-glucan recognition receptors and the inflammatory proteases caspase-8 and caspase-1 in coordinating cytokine secretion and cell death in response to immunostimulatory fungal components.
82	25063877	Caspase-8 modulates dectin-1 and complement receptor 3-driven IL-1β production in response to β-glucans and the fungal pathogen, Candida albicans.
83	25063877	The nucleotide-binding domain and leucine-rich repeat containing family (NLR), pyrin domain-containing 3 (NLRP3) inflammasome plays a key role in triggering caspase-1-dependent IL-1β maturation and resistance to fungal dissemination in Candida albicans infection. β-Glucans are major components of fungal cell walls that trigger IL-1β secretion in both murine and human immune cells.
84	25063877	We show that the NLRP3-apoptosis-associated speck-like protein containing caspase recruitment domain protein-caspase-1 inflammasome is absolutely critical for IL-1β production in response to β-glucans.
85	25063877	Interestingly, we also found that both complement receptor 3 (CR3) and dectin-1 play a crucial role in coordinating β-glucan-induced IL-1β processing as well as a cell death response.
86	25063877	In addition to the essential role of caspase-1, we identify an important role for the proapoptotic protease caspase-8 in promoting β-glucan-induced cell death and NLRP3 inflammasome-dependent IL-1β maturation.
87	25063877	A strong requirement for CR3 and caspase-8 also was found for NLRP3-dependent IL-1β production in response to heat-killed C. albicans.
88	25063877	Taken together, these results define the importance of dectin-1, CR3, and caspase-8, in addition to the canonical NLRP3 inflammasome, in mediating β-glucan- and C. albicans-induced innate responses in dendritic cells.
89	25063877	Collectively, these findings establish a novel link between β-glucan recognition receptors and the inflammatory proteases caspase-8 and caspase-1 in coordinating cytokine secretion and cell death in response to immunostimulatory fungal components.
90	25453580	However, recognition of β-glucans appeared cell type-specific as both dectin-1 and CR3 are involved in the β-glucan-mediated responses in pig macrophages.