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CD4 — IL21

Text-mined interactions from Literome

Pepe et al., Curr Pharm Des 2006 : This Th1 polarizing activity is mediated by interleukin-12 released by infected CDs in the presence of CD4 ( + ) cells
Peluso et al., J Immunol 2007 : We therefore examined whether IL-21 controls CD4 ( + ) CD25 ( + ) T cell function ... Additionally, CD4 ( + ) CD25 ( + ) T cells induced in the presence of IL-21 maintain the ability to suppress alloresponses
Ariga et al., Immunology 2007 : Using T-cell receptor ( TCR ) transgenic mice, we demonstrate that TCR stimulation of naive CD4 ( + ) T cells induces transient T-bet expression, interleukin (IL)-12 receptor beta2 up-regulation, and GATA-3 down-regulation, which leads to T helper ( Th ) 1 differentiation even when the cells are stimulated with peptide loaded I-A ( b ) -transfected Chinese hamster ovary cells in the absence of interferon-gamma (IFN-gamma) and IL-12
Kuchen et al., J Immunol 2007 : Finally, IL-21R-Fc did not inhibit anti-CD3 induced CD4 ( + ) T cell activation, but rather directly blocked T cell induced B cell activation and PC differentiation
Liu et al., Inflamm Bowel Dis 2009 (Inflammatory Bowel Diseases) : IL-21 enhances IBD NK cell cytotoxic response, triggers T cells to produce proinflammatory cytokines, and induces IBD CD4 ( + ) T cells to differentiate into Th17 cells, suggesting that IL-21 is involved in the pathogenesis of IBD and that blocking IL-21R signaling may have a therapeutic potential in IBD
Li et al., J Immunol 2009 (Encephalomyelitis, Autoimmune, Experimental) : However, E-FABP-deficient CD4 ( + ) T cells expressed significantly higher levels of the nuclear receptor peroxisome proliferator activating receptor ( PPAR)gamma than did wild-type CD4 ( + ) T cells, and treatment with the PPARgamma antagonist GW9662 restored expression of IL-21 , RORgammat, RORalpha, and IL-17 by E-FABP-deficient T cells to wild-type levels
Ertelt et al., Immunology 2010 (Listeriosis) : Unexpectedly however, IL-21 deficiency caused significantly increased CD4 ( + ) T-cell IL-17 production, and this effect became even more pronounced after L. monocytogenes infection in mice with combined defects in both IL-12 and type I IFN receptor that develop a T helper type 17-dominated CD4 ( + ) T-cell response
Liu et al., Cell Immunol 2011 : Further analysis indicated that IL-21 induced phosphorylation of STAT1, STAT3 and STAT5 in activated naïve CD4 ( + ) T cells
Maddur et al., J Clin Immunol 2013 : Naive CD4 ( + ) T cells were stimulated in the presence of TGF-ß, IL-21 , and IL-23 for the differentiation of Th17 cells
Dodd et al., Mucosal Immunol 2013 (Respiratory Syncytial Virus Infections) : Endogenous IL-21 regulates pathogenic mucosal CD4 T-cell responses during enhanced RSV disease in mice
Vandergeeten et al., Blood 2013 (HIV Infections) : When administered to HIV infected subjects receiving suppressive ART, interleukin-7 (IL-7) increases the number of CD4 ( + ) T cells by promoting their survival and proliferation
Suzuki et al., J Virol 1999 : Among them, interleukin-12 (IL-12) and IL-4 induce naive CD4 ( + ) T cells to become T-helper 1 ( Th1 ) or Th2 cells, respectively