Ignet

Gene Information

Gene symbol: PRDM1

Gene name: PR domain containing 1, with ZNF domain

HGNC ID: 9346

Synonyms: PRDI-BF1

Related Genes

#	Gene Symbol	Number of hits
1	AICDA	1 hits
2	BCL6	1 hits
3	CD4	1 hits
4	CD40	1 hits
5	CD8A	1 hits
6	CXCR4	1 hits
7	CXCR5	1 hits
8	CYP1B1	1 hits
9	HLA-A	1 hits
10	ICOS	1 hits
11	IFNG	1 hits
12	IL17C	1 hits
13	IL2	1 hits
14	IRF4	1 hits
15	MAPK1	1 hits
16	MTA3	1 hits
17	NFATC1	1 hits
18	NFKB1	1 hits
19	PAX5	1 hits
20	PDCD1	1 hits
21	PTGS2	1 hits
22	SH2D1A	1 hits
23	STAT5A	1 hits
24	TBX21	1 hits
25	XBP1	1 hits
26	XBPP1	1 hits

Related Sentences

#	PMID	Sentence
1	11877292	The results show that a variety of differentiation molecules, proteins involved in the control of apoptosis, the B-cell transcription factors, positive regulatory domain I-binding factor 1/B lymphocyte-induced maturation protein 1 and B cell-specific activating protein and, at least partially, the chemokine receptor CXCR4 were expressed by human PCs following a gradient of increasing maturity in the direction: tonsil-->blood-->BM.
2	15663361	And, finally, we show that there is no change in NF-kappaB or Blimp-1 in old vs young stimulated B cells.
3	17339456	We show that immature and transitional 1 (immature/T1) B cells constitutively express activation-induced cytidine deaminase and B lymphocyte-induced maturation protein 1 in amounts that support accelerated plasmacytic differentiation and limited class-switch recombination.
4	19201852	In response to TLR7/8 stimulation, PDCs mediated the up-regulation of transcription factors B lymphocyte-induced maturation protein 1 and X-box binding protein 1 and enhanced differentiation of B cells into IgM-, IgG-, and IgA-producing cells.
5	19201852	Although MDCs expressed higher levels of the known B cell growth factors IL-6, IL-10, and B cell-activating factor in response to TLR7/8 stimulation, they were unable to enhance B cell responses in this system.
6	19201852	These data help decipher the different roles of PDCs and MDCs for modulating human B cell responses and can contribute to selection of specific TLR ligands as vaccine adjuvants.
7	19376580	VLPs stimulated the proliferation of B220(+)IgM(+)CD43(-)CD5(-) B2 cells and their differentiation to plasma cells that preferentially produce IgG2a antibodies.
8	19376580	Up-regulation of Blimp-1, XBP-1, IRF4, and AID genes, which are responsible for class-switch recombination and somatic hypermutation, was observed in VLP-activated B2 cells.
9	19376580	Stimulation of naïve splenocytes with VLPs led to a high expression of IL-12, RANTES and MIP, the cytokine milieu that favors B cell differentiation into IgG2a secreting cells.
10	19540920	The Escherichia coli produced recombinant IL-2 was shown to increase the expression of two transcription factors, STAT5 and Blimp-1, known to be involved in IL-2 signalling in mammals, as well as IFN-gamma, gIP and IL-2 itself.
11	19608860	Bcl6 and Blimp-1 are reciprocal and antagonistic regulators of T follicular helper cell differentiation.
12	19608860	We found that expression of the transcription factor Bcl6 in CD4+ T cells is both necessary and sufficient for in vivo T(FH) differentiation and T cell help to B cells in mice.
13	19608860	In contrast, the transcription factor Blimp-1, an antagonist of Bcl6, inhibits T(FH) differentiation and help, thereby preventing B cell germinal center and antibody responses.
14	19608860	These findings demonstrate that T(FH) cells are required for proper B cell responses in vivo and that Bcl6 and Blimp-1 play central but opposing roles in T(FH) differentiation.
15	19608860	Bcl6 and Blimp-1 are reciprocal and antagonistic regulators of T follicular helper cell differentiation.
16	19608860	We found that expression of the transcription factor Bcl6 in CD4+ T cells is both necessary and sufficient for in vivo T(FH) differentiation and T cell help to B cells in mice.
17	19608860	In contrast, the transcription factor Blimp-1, an antagonist of Bcl6, inhibits T(FH) differentiation and help, thereby preventing B cell germinal center and antibody responses.
18	19608860	These findings demonstrate that T(FH) cells are required for proper B cell responses in vivo and that Bcl6 and Blimp-1 play central but opposing roles in T(FH) differentiation.
19	19608860	Bcl6 and Blimp-1 are reciprocal and antagonistic regulators of T follicular helper cell differentiation.
20	19608860	We found that expression of the transcription factor Bcl6 in CD4+ T cells is both necessary and sufficient for in vivo T(FH) differentiation and T cell help to B cells in mice.
21	19608860	In contrast, the transcription factor Blimp-1, an antagonist of Bcl6, inhibits T(FH) differentiation and help, thereby preventing B cell germinal center and antibody responses.
22	19608860	These findings demonstrate that T(FH) cells are required for proper B cell responses in vivo and that Bcl6 and Blimp-1 play central but opposing roles in T(FH) differentiation.
23	20050331	We demonstrate that the Cox-2 selective small molecule inhibitors SC-58125 and NS-398 attenuate the production of human antibody isotypes including immunoglobulin M (IgM), IgG1, IgG2, IgG3 and IgG4.
24	20050331	In addition, inhibition of Cox-2 significantly reduced the generation of CD38+ IgM+ and CD38+ IgG+ antibody-secreting cells.
25	20050331	Interestingly, we discovered that inhibition of Cox-2 activity in normal human B cells severely reduced the messenger RNA and protein levels of the essential plasma cell transcription factor, Blimp-1.
26	20050331	These observations were mirrored in Cox-2-deficient mice, which had reduced CD138+ plasma cells and a near loss of Blimp-1 expression.
27	20050331	We demonstrate that the Cox-2 selective small molecule inhibitors SC-58125 and NS-398 attenuate the production of human antibody isotypes including immunoglobulin M (IgM), IgG1, IgG2, IgG3 and IgG4.
28	20050331	In addition, inhibition of Cox-2 significantly reduced the generation of CD38+ IgM+ and CD38+ IgG+ antibody-secreting cells.
29	20050331	Interestingly, we discovered that inhibition of Cox-2 activity in normal human B cells severely reduced the messenger RNA and protein levels of the essential plasma cell transcription factor, Blimp-1.
30	20050331	These observations were mirrored in Cox-2-deficient mice, which had reduced CD138+ plasma cells and a near loss of Blimp-1 expression.
31	20084069	Effectors and memories: Bcl-6 and Blimp-1 in T and B lymphocyte differentiation.
32	20084069	Bcl-6 and Blimp-1 have recently been identified as key transcriptional regulators of effector and memory differentiation in CD4(+) T cells and CD8(+) T cells.
33	20084069	Bcl-6 and Blimp-1 were previously known to be critical regulators of effector and memory differentiation of B lymphocytes.
34	20084069	The new findings unexpectedly point to the Bcl-6 and Blimp-1 regulatory axis as a ubiquitous mechanism for controlling effector and memory lymphocyte differentiation and function.
35	20084069	Bcl-6 and Blimp-1 are antagonistic transcription factors and can function as a self-reinforcing genetic switch for cell-fate decisions.
36	20084069	Here we review and examine the commonalities and differences in the functions of these transcription factors in CD4(+) follicular helper T(FH) lymphocytes, effector CD8(+) T lymphocytes and B lymphocytes.
37	20084069	Effectors and memories: Bcl-6 and Blimp-1 in T and B lymphocyte differentiation.
38	20084069	Bcl-6 and Blimp-1 have recently been identified as key transcriptional regulators of effector and memory differentiation in CD4(+) T cells and CD8(+) T cells.
39	20084069	Bcl-6 and Blimp-1 were previously known to be critical regulators of effector and memory differentiation of B lymphocytes.
40	20084069	The new findings unexpectedly point to the Bcl-6 and Blimp-1 regulatory axis as a ubiquitous mechanism for controlling effector and memory lymphocyte differentiation and function.
41	20084069	Bcl-6 and Blimp-1 are antagonistic transcription factors and can function as a self-reinforcing genetic switch for cell-fate decisions.
42	20084069	Here we review and examine the commonalities and differences in the functions of these transcription factors in CD4(+) follicular helper T(FH) lymphocytes, effector CD8(+) T lymphocytes and B lymphocytes.
43	20084069	Effectors and memories: Bcl-6 and Blimp-1 in T and B lymphocyte differentiation.
44	20084069	Bcl-6 and Blimp-1 have recently been identified as key transcriptional regulators of effector and memory differentiation in CD4(+) T cells and CD8(+) T cells.
45	20084069	Bcl-6 and Blimp-1 were previously known to be critical regulators of effector and memory differentiation of B lymphocytes.
46	20084069	The new findings unexpectedly point to the Bcl-6 and Blimp-1 regulatory axis as a ubiquitous mechanism for controlling effector and memory lymphocyte differentiation and function.
47	20084069	Bcl-6 and Blimp-1 are antagonistic transcription factors and can function as a self-reinforcing genetic switch for cell-fate decisions.
48	20084069	Here we review and examine the commonalities and differences in the functions of these transcription factors in CD4(+) follicular helper T(FH) lymphocytes, effector CD8(+) T lymphocytes and B lymphocytes.
49	20084069	Effectors and memories: Bcl-6 and Blimp-1 in T and B lymphocyte differentiation.
50	20084069	Bcl-6 and Blimp-1 have recently been identified as key transcriptional regulators of effector and memory differentiation in CD4(+) T cells and CD8(+) T cells.
51	20084069	Bcl-6 and Blimp-1 were previously known to be critical regulators of effector and memory differentiation of B lymphocytes.
52	20084069	The new findings unexpectedly point to the Bcl-6 and Blimp-1 regulatory axis as a ubiquitous mechanism for controlling effector and memory lymphocyte differentiation and function.
53	20084069	Bcl-6 and Blimp-1 are antagonistic transcription factors and can function as a self-reinforcing genetic switch for cell-fate decisions.
54	20084069	Here we review and examine the commonalities and differences in the functions of these transcription factors in CD4(+) follicular helper T(FH) lymphocytes, effector CD8(+) T lymphocytes and B lymphocytes.
55	20084069	Effectors and memories: Bcl-6 and Blimp-1 in T and B lymphocyte differentiation.
56	20084069	Bcl-6 and Blimp-1 have recently been identified as key transcriptional regulators of effector and memory differentiation in CD4(+) T cells and CD8(+) T cells.
57	20084069	Bcl-6 and Blimp-1 were previously known to be critical regulators of effector and memory differentiation of B lymphocytes.
58	20084069	The new findings unexpectedly point to the Bcl-6 and Blimp-1 regulatory axis as a ubiquitous mechanism for controlling effector and memory lymphocyte differentiation and function.
59	20084069	Bcl-6 and Blimp-1 are antagonistic transcription factors and can function as a self-reinforcing genetic switch for cell-fate decisions.
60	20084069	Here we review and examine the commonalities and differences in the functions of these transcription factors in CD4(+) follicular helper T(FH) lymphocytes, effector CD8(+) T lymphocytes and B lymphocytes.
61	21314428	Distinguishing features of T(FH) cells are the expression of CXCR5, PD-1, SAP (SH2D1A), IL-21, and ICOS, among other molecules, and the absence of Blimp-1 (prdm1).
62	21894172	Immunoglobulin light chain, Blimp-1 and cytochrome P4501B1 peptides as potential vaccines for AL amyloidosis.
63	21894172	Three peptide/MHC I-binding algorithms identified immunogenic peptides from three AL plasma cell-associated proteins: (1) amyloidogenic λ6 light chains, (2) CYP1B1, a universal tumor antigen hyper-expressed in AL plasma cells and (3) B lymphocyte-induced maturation protein 1 (Blimp-1), a transcription factor required for plasma cell differentiation.
64	21894172	Immunoglobulin light chain, Blimp-1 and cytochrome P4501B1 peptides as potential vaccines for AL amyloidosis.
65	21894172	Three peptide/MHC I-binding algorithms identified immunogenic peptides from three AL plasma cell-associated proteins: (1) amyloidogenic λ6 light chains, (2) CYP1B1, a universal tumor antigen hyper-expressed in AL plasma cells and (3) B lymphocyte-induced maturation protein 1 (Blimp-1), a transcription factor required for plasma cell differentiation.
66	22271576	Constitutive STAT5 signaling in activated CD4(+) T cells selectively blocked T(FH) cell differentiation and GCs, and IL-2 signaling was a primary inducer of this pathway.
67	22271576	Conversely, STAT5-deficient CD4(+) T cells (mature STAT5(fl/fl) CD4(+) T cells transduced with a Cre-expressing vector) rapidly up-regulated Bcl6 expression and preferentially differentiated into T(FH) cells during T cell priming in vivo.
68	22271576	These results demonstrate that IL-2, STAT5, and Blimp-1 collaborate to negatively regulate T(FH) cell differentiation.
69	22948808	Phenotype and function of protective, CD4-independent CD8 T cell memory.
70	22948808	While the need for CD4 T cells in the generation of CD8 T cell memory has been well documented, the mechanism underlying their requirement remains unknown.
71	22948808	Here, we detail an immunization method capable of generating CD8 memory T cells that are indifferent to CD4 T cell help.
72	22948808	Using a subunit vaccination that combines polyIC and an agonistic CD40 antibody, we program protective CD4-independent CD8 T cell memory.
73	22948808	When cells generated by combined polyIC/CD40 immunization are compared to cells produced following a CD4-dependent vaccination, Listeria monocytogenes, they display dramatic differences, both phenotypically and functionally.
74	22948808	The memory cells generated in a CD4-deficient host by polyIC/CD40 immunization provide protection against secondary infectious challenge, whereas cells generated by LM immunization in the same environment do not.
75	22948808	Interestingly, combined polyIC/CD40 immunization generates long-term memory cells with low Blimp-1 and elevated Eomes expression despite high expression of Blimp-1 during the primary response.
76	22948808	The potency of combined polyIC/CD40 to elicit CD8+ T cell memory in the absence of CD4 T cells suggests that it could be considered as a vaccine adjuvant in clinical situations where CD4 responses/numbers are compromised.
77	23816303	In the present study, we have used isolated purified B cells and in vivo studies to demonstrate that αGalCer and RA initiate a regulated expression of several genes essential for B cell activation and differentiation, such as Pax-5, Blimp-1, IRF-4 and activation-induced cytidine deaminase (Aid).
78	23816303	Moreover, whereas αGalCer mainly increased the expression of Pax-5, CD40 and CD86 that are critical for B cell activation, RA predominantly increased CD138⁺ and Fas⁺-PNA⁺ B cells, which represent more advanced B cell differentiation.
79	24590765	Blimp-1 represses CD8 T cell expression of PD-1 using a feed-forward transcriptional circuit during acute viral infection.
80	24590765	We show here that B lymphocyte-induced maturation protein 1 (Blimp-1)-deficient CD8 T cells fail to repress PD-1 during the early stages of CD8 T cell differentiation after acute infection with lymphocytic choriomeningitis virus (LCMV) strain Armstrong.
81	24590765	Blimp-1 represses PD-1 through a feed-forward repressive circuit by regulating PD-1 directly and by repressing NFATc1 expression, an activator of PD-1 expression.
82	24590765	Blimp-1 binding induces a repressive chromatin structure at the PD-1 locus, leading to the eviction of NFATc1 from its site.
83	24590765	These data place Blimp-1 at an important phase of the CD8 T cell effector response and provide a molecular mechanism for its repression of PD-1.
84	24590765	Blimp-1 represses CD8 T cell expression of PD-1 using a feed-forward transcriptional circuit during acute viral infection.
85	24590765	We show here that B lymphocyte-induced maturation protein 1 (Blimp-1)-deficient CD8 T cells fail to repress PD-1 during the early stages of CD8 T cell differentiation after acute infection with lymphocytic choriomeningitis virus (LCMV) strain Armstrong.
86	24590765	Blimp-1 represses PD-1 through a feed-forward repressive circuit by regulating PD-1 directly and by repressing NFATc1 expression, an activator of PD-1 expression.
87	24590765	Blimp-1 binding induces a repressive chromatin structure at the PD-1 locus, leading to the eviction of NFATc1 from its site.
88	24590765	These data place Blimp-1 at an important phase of the CD8 T cell effector response and provide a molecular mechanism for its repression of PD-1.
89	24590765	Blimp-1 represses CD8 T cell expression of PD-1 using a feed-forward transcriptional circuit during acute viral infection.
90	24590765	We show here that B lymphocyte-induced maturation protein 1 (Blimp-1)-deficient CD8 T cells fail to repress PD-1 during the early stages of CD8 T cell differentiation after acute infection with lymphocytic choriomeningitis virus (LCMV) strain Armstrong.
91	24590765	Blimp-1 represses PD-1 through a feed-forward repressive circuit by regulating PD-1 directly and by repressing NFATc1 expression, an activator of PD-1 expression.
92	24590765	Blimp-1 binding induces a repressive chromatin structure at the PD-1 locus, leading to the eviction of NFATc1 from its site.
93	24590765	These data place Blimp-1 at an important phase of the CD8 T cell effector response and provide a molecular mechanism for its repression of PD-1.
94	24590765	Blimp-1 represses CD8 T cell expression of PD-1 using a feed-forward transcriptional circuit during acute viral infection.
95	24590765	We show here that B lymphocyte-induced maturation protein 1 (Blimp-1)-deficient CD8 T cells fail to repress PD-1 during the early stages of CD8 T cell differentiation after acute infection with lymphocytic choriomeningitis virus (LCMV) strain Armstrong.
96	24590765	Blimp-1 represses PD-1 through a feed-forward repressive circuit by regulating PD-1 directly and by repressing NFATc1 expression, an activator of PD-1 expression.
97	24590765	Blimp-1 binding induces a repressive chromatin structure at the PD-1 locus, leading to the eviction of NFATc1 from its site.
98	24590765	These data place Blimp-1 at an important phase of the CD8 T cell effector response and provide a molecular mechanism for its repression of PD-1.
99	24590765	Blimp-1 represses CD8 T cell expression of PD-1 using a feed-forward transcriptional circuit during acute viral infection.
100	24590765	We show here that B lymphocyte-induced maturation protein 1 (Blimp-1)-deficient CD8 T cells fail to repress PD-1 during the early stages of CD8 T cell differentiation after acute infection with lymphocytic choriomeningitis virus (LCMV) strain Armstrong.
101	24590765	Blimp-1 represses PD-1 through a feed-forward repressive circuit by regulating PD-1 directly and by repressing NFATc1 expression, an activator of PD-1 expression.
102	24590765	Blimp-1 binding induces a repressive chromatin structure at the PD-1 locus, leading to the eviction of NFATc1 from its site.
103	24590765	These data place Blimp-1 at an important phase of the CD8 T cell effector response and provide a molecular mechanism for its repression of PD-1.
104	24837104	Distinct underlying mechanisms of altered survival and differentiation were revealed with the latter regulated by the transcription factors T-bet and Blimp-1.
105	25012778	Cyclooxygenase inhibitors inhibit antibody response through interference with MAPK/ERK pathways and BLIMP-1 inhibition.
106	25015830	IL-2 induction of Blimp-1 is a key in vivo signal for CD8+ short-lived effector T cell differentiation.
107	25015830	However, it has been shown that cytokines such as IL-2 induce Blimp-1 expression in vitro.
108	25015830	In this study, we took advantage of the low-inflammation model of dendritic cell immunization to study the role of the IL-2/Blimp-1 axis in SLEC differentiation as well as the importance of Blimp-1 expression in memory precursor effector cells for proper CD8(+) memory generation.
109	25015830	In addition, modulation of the bioavailability of IL-2 by injection either of a blocking Ab or of the cytokine, demonstrates a link between IL-2, Blimp-1 induction, and SLEC formation in wild-type cells.
110	25015830	Conversely, injection of IL-2 had less effect on Blimp-1-deficient CD8(+) T cells, indicating that the effect of IL-2 on in vivo SLEC differentiation is mediated by Blimp-1.
111	25015830	In conclusion, IL-2 induction of Blimp-1 expression is a key regulator of SLEC differentiation in vivo.
112	25015830	IL-2 induction of Blimp-1 is a key in vivo signal for CD8+ short-lived effector T cell differentiation.
113	25015830	However, it has been shown that cytokines such as IL-2 induce Blimp-1 expression in vitro.
114	25015830	In this study, we took advantage of the low-inflammation model of dendritic cell immunization to study the role of the IL-2/Blimp-1 axis in SLEC differentiation as well as the importance of Blimp-1 expression in memory precursor effector cells for proper CD8(+) memory generation.
115	25015830	In addition, modulation of the bioavailability of IL-2 by injection either of a blocking Ab or of the cytokine, demonstrates a link between IL-2, Blimp-1 induction, and SLEC formation in wild-type cells.
116	25015830	Conversely, injection of IL-2 had less effect on Blimp-1-deficient CD8(+) T cells, indicating that the effect of IL-2 on in vivo SLEC differentiation is mediated by Blimp-1.
117	25015830	In conclusion, IL-2 induction of Blimp-1 expression is a key regulator of SLEC differentiation in vivo.
118	25015830	IL-2 induction of Blimp-1 is a key in vivo signal for CD8+ short-lived effector T cell differentiation.
119	25015830	However, it has been shown that cytokines such as IL-2 induce Blimp-1 expression in vitro.
120	25015830	In this study, we took advantage of the low-inflammation model of dendritic cell immunization to study the role of the IL-2/Blimp-1 axis in SLEC differentiation as well as the importance of Blimp-1 expression in memory precursor effector cells for proper CD8(+) memory generation.
121	25015830	In addition, modulation of the bioavailability of IL-2 by injection either of a blocking Ab or of the cytokine, demonstrates a link between IL-2, Blimp-1 induction, and SLEC formation in wild-type cells.
122	25015830	Conversely, injection of IL-2 had less effect on Blimp-1-deficient CD8(+) T cells, indicating that the effect of IL-2 on in vivo SLEC differentiation is mediated by Blimp-1.
123	25015830	In conclusion, IL-2 induction of Blimp-1 expression is a key regulator of SLEC differentiation in vivo.
124	25015830	IL-2 induction of Blimp-1 is a key in vivo signal for CD8+ short-lived effector T cell differentiation.
125	25015830	However, it has been shown that cytokines such as IL-2 induce Blimp-1 expression in vitro.
126	25015830	In this study, we took advantage of the low-inflammation model of dendritic cell immunization to study the role of the IL-2/Blimp-1 axis in SLEC differentiation as well as the importance of Blimp-1 expression in memory precursor effector cells for proper CD8(+) memory generation.
127	25015830	In addition, modulation of the bioavailability of IL-2 by injection either of a blocking Ab or of the cytokine, demonstrates a link between IL-2, Blimp-1 induction, and SLEC formation in wild-type cells.
128	25015830	Conversely, injection of IL-2 had less effect on Blimp-1-deficient CD8(+) T cells, indicating that the effect of IL-2 on in vivo SLEC differentiation is mediated by Blimp-1.
129	25015830	In conclusion, IL-2 induction of Blimp-1 expression is a key regulator of SLEC differentiation in vivo.
130	25015830	IL-2 induction of Blimp-1 is a key in vivo signal for CD8+ short-lived effector T cell differentiation.
131	25015830	However, it has been shown that cytokines such as IL-2 induce Blimp-1 expression in vitro.
132	25015830	In this study, we took advantage of the low-inflammation model of dendritic cell immunization to study the role of the IL-2/Blimp-1 axis in SLEC differentiation as well as the importance of Blimp-1 expression in memory precursor effector cells for proper CD8(+) memory generation.
133	25015830	In addition, modulation of the bioavailability of IL-2 by injection either of a blocking Ab or of the cytokine, demonstrates a link between IL-2, Blimp-1 induction, and SLEC formation in wild-type cells.
134	25015830	Conversely, injection of IL-2 had less effect on Blimp-1-deficient CD8(+) T cells, indicating that the effect of IL-2 on in vivo SLEC differentiation is mediated by Blimp-1.
135	25015830	In conclusion, IL-2 induction of Blimp-1 expression is a key regulator of SLEC differentiation in vivo.
136	25015830	IL-2 induction of Blimp-1 is a key in vivo signal for CD8+ short-lived effector T cell differentiation.
137	25015830	However, it has been shown that cytokines such as IL-2 induce Blimp-1 expression in vitro.
138	25015830	In this study, we took advantage of the low-inflammation model of dendritic cell immunization to study the role of the IL-2/Blimp-1 axis in SLEC differentiation as well as the importance of Blimp-1 expression in memory precursor effector cells for proper CD8(+) memory generation.
139	25015830	In addition, modulation of the bioavailability of IL-2 by injection either of a blocking Ab or of the cytokine, demonstrates a link between IL-2, Blimp-1 induction, and SLEC formation in wild-type cells.
140	25015830	Conversely, injection of IL-2 had less effect on Blimp-1-deficient CD8(+) T cells, indicating that the effect of IL-2 on in vivo SLEC differentiation is mediated by Blimp-1.
141	25015830	In conclusion, IL-2 induction of Blimp-1 expression is a key regulator of SLEC differentiation in vivo.
142	26460037	Bcl6 middle domain repressor function is required for T follicular helper cell differentiation and utilizes the corepressor MTA3.
143	26460037	Mimicked acetylation of the Bcl6 middle domain (K379Q) in CD4 T cells results in significant reductions in Tfh differentiation in vivo.
144	26460037	Although Bcl6 K379Q still bound to the Prdm1 cis-regulatory elements in Tfh cells, Prdm1 expression was derepressed.
145	26460037	This was a result of the failure of Bcl6 K379Q to recruit metastasis-associated protein 3 (MTA3).
146	26460037	The loss of Bcl6 function in Bcl6 K379Q-expressing CD4 T cells could be partially rescued by abrogating Prdm1 expression.
147	26460037	In addition to Prdm1, we found that Bcl6 recruits MTA3 to multiple genes involved in Tfh cell biology, including genes important for cell migration, cell survival, and alternative differentiation pathways.
148	26460037	Thus, Bcl6 middle domain mediated repression is a major mechanism of action by which Bcl6 controls CD4 T-cell fate and function.
149	26460037	Bcl6 middle domain repressor function is required for T follicular helper cell differentiation and utilizes the corepressor MTA3.
150	26460037	Mimicked acetylation of the Bcl6 middle domain (K379Q) in CD4 T cells results in significant reductions in Tfh differentiation in vivo.
151	26460037	Although Bcl6 K379Q still bound to the Prdm1 cis-regulatory elements in Tfh cells, Prdm1 expression was derepressed.
152	26460037	This was a result of the failure of Bcl6 K379Q to recruit metastasis-associated protein 3 (MTA3).
153	26460037	The loss of Bcl6 function in Bcl6 K379Q-expressing CD4 T cells could be partially rescued by abrogating Prdm1 expression.
154	26460037	In addition to Prdm1, we found that Bcl6 recruits MTA3 to multiple genes involved in Tfh cell biology, including genes important for cell migration, cell survival, and alternative differentiation pathways.
155	26460037	Thus, Bcl6 middle domain mediated repression is a major mechanism of action by which Bcl6 controls CD4 T-cell fate and function.
156	26460037	Bcl6 middle domain repressor function is required for T follicular helper cell differentiation and utilizes the corepressor MTA3.
157	26460037	Mimicked acetylation of the Bcl6 middle domain (K379Q) in CD4 T cells results in significant reductions in Tfh differentiation in vivo.
158	26460037	Although Bcl6 K379Q still bound to the Prdm1 cis-regulatory elements in Tfh cells, Prdm1 expression was derepressed.
159	26460037	This was a result of the failure of Bcl6 K379Q to recruit metastasis-associated protein 3 (MTA3).
160	26460037	The loss of Bcl6 function in Bcl6 K379Q-expressing CD4 T cells could be partially rescued by abrogating Prdm1 expression.
161	26460037	In addition to Prdm1, we found that Bcl6 recruits MTA3 to multiple genes involved in Tfh cell biology, including genes important for cell migration, cell survival, and alternative differentiation pathways.
162	26460037	Thus, Bcl6 middle domain mediated repression is a major mechanism of action by which Bcl6 controls CD4 T-cell fate and function.