Browsing by keyword "Animals; Apoptosis; Calcium-Calmodulin-Dependent Protein Kinases; Cell Differentiation; Cell Division; DNA-Binding Proteins; Female; Gene Targeting; Hemocyanin; Interferon Type II; Interleukins; JNK Mitogen-Activated Protein Kinases; *Lymphocyte Activation; Male; Mice; Mice, Knockout; *Mitogen-Activated Protein Kinases; NFATC Transcription Factors; *Nuclear Proteins; Signal Transduction; T-Lymphocytes, Helper-Inducer; Th1 Cells; Th2 Cells; Transcription Factors"
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Defective T cell differentiation in the absence of Jnk1The c-Jun NH2-terminal kinase (JNK) signaling pathway has been implicated in the immune response that is mediated by the activation and differentiation of CD4 helper T (TH) cells into TH1 and TH2 effector cells. JNK activity observed in wild-type activated TH cells was severely reduced in TH cells from Jnk1-/- mice. The Jnk1-/- T cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differentiated to TH2 cells. The enhanced production of TH2 cytokines by Jnk1-/- cells was associated with increased nuclear accumulation of the transcription factor NFATc. Thus, the JNK1 signaling pathway plays a key role in T cell receptor-initiated TH cell proliferation, apoptosis, and differentiation.