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CCNG1 — IL2

Text-mined interactions from Literome

D'Souza et al., J Immunol 2003 (Stomatitis) : IL-2 is not required for the initiation of CD8 T cell cycling but sustains expansion
Dooms et al., J Immunol 2004 : We show that Ag-induced cycling of CD4 ( + ) IL-2 ( -/- ) T cells is independent of IL-2 in vitro
Kaminitz et al., PloS one 2011 : Proliferation rates and sensitivity to Fas cross linking are dissociated in Treg cells : fast cycling induced by IL-2 and CD3/CD28 stimulation improve Treg resistance to Fas-ligand (FasL) in both strains
Critchfield et al., Science 1994 (Encephalomyelitis, Autoimmune, Experimental) : T cell death was shown to be a physiological response to interleukin-2 stimulated cell cycling and T cell receptor reengagement at high antigen doses
Clements et al., Int Immunol 1993 (Lymphoproliferative Disorders) : These data show that the hyporesponsiveness of lpr CD4-CD8- T cells does not result from a lack of CD28 expression, that it is not a fixed state, and that it can be reversed by the induction of cell cycling in the presence of IL-2
Budd et al., Semin Immunol 1994 (Lymphoproliferative Disorders) : Finally, lpr CD4-8- T cells bear many similarities to anergic T cells, including high expression of p59fyn, lack of IL-2 production, and recovery of function following induction of cell cycling in the presence of IL-2
Racke et al., Ann Neurol 1996 (Encephalomyelitis, Autoimmune, Experimental...) : These studies showed that although interleukin-2 stimulated cell cycling is an important factor leading to T-cell death, the administration of exogenous interleukin-2 with antigen can result in the aggravation of clinical disease compared to administration of antigen alone
Zheng et al., J Immunol 1998 : TCR stimulation of T lymphocytes that are activated and cycling in the presence of IL-2 leads to programmed cell death