期刊
CELL
卷 109, 期 6, 页码 719-731出版社
CELL PRESS
DOI: 10.1016/S0092-8674(02)00767-5
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资金
- NCI NIH HHS [CA42471] Funding Source: Medline
- NIAID NIH HHS [AI48213] Funding Source: Medline
In lymphocytes, integration of Call and other signaling pathways results in productive activation, while unopposed Call signaling leads to tolerance or anergy. We show that the Ca2+-regulated transcription factor NFAT has an integral role in both aspects of lymphocyte function. Ca2+/calcineurin signaling induces a limited set of anergy-associated genes, distinct from genes induced in the productive immune response; these genes are upregulated in vivo in tolerant T cells and are largely NFAT dependent. T cells lacking NFAT1 are resistant to anergy induction; conversely, NFAT1 induces T cell anergy if prevented from interacting with its transcriptional partner AP-1 (Fos/Jun). Thus, in the absence of AP-1, NFAT imposes a genetic program of lymphocyte anergy that counters the program of productive activation mediated by the cooperative NFAT:AP-1 complex.
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