期刊
IMMUNOLOGICAL REVIEWS
卷 229, 期 -, 页码 12-26出版社
WILEY
DOI: 10.1111/j.1600-065X.2009.00770.x
关键词
CD28; CTLA-4; TRIM; PKB; AKT; apoptosis
类别
资金
- Biotechnology and Biological Sciences Research Council [BB/E015395/1] Funding Source: Medline
- Wellcome Trust [060111] Funding Source: Medline
- BBSRC [BB/E015395/1] Funding Source: UKRI
T-cell activation is mediated by antigen-specific signals from the TCR zeta/CD3 and CD4-CD8-p56lck complexes in combination with additional co-signals provided by coreceptors such as CD28, inducible costimulator (ICOS), cytotoxic T-lymphocyte antigen-4 (CTLA-4), programmed death (PD-1), and others. CD28 and ICOS provide positive signals that promote and sustain T-cell responses, while CTLA-4 and PD-1 limit responses. The balance between stimulatory and inhibitory co-signals determines the ultimate nature of T-cell responses where response to foreign pathogen is achieved without excess inflammation and autoimmunity. In this review, we outline the current knowledge of the CD28 and CTLA-4 signaling mechanisms [involving phosphatidylinositol 3 kinase (PI3K), growth factor receptor-bound protein 2 (Grb2), Filamin A, protein kinase C theta (PKC theta), and phosphatases] that control T-cell immunity. We also present recent findings on T-cell receptor-interacting molecule (TRIM) regulation of CTLA-4 surface expression, and a signaling pathway involving CTLA-4 activation of PI3K and protein kinase B (PKB)/AKT by which cell survival is ensured under conditions of anergy induction.
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