期刊
NATURE IMMUNOLOGY
卷 10, 期 1, 页码 92-100出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1673
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资金
- NCI NIH HHS [R01 CA100850, CA78656, CA87583, R01 CA134807, R01 CA087583] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA100850, R01CA134807, K08CA078656, R01CA087583] Funding Source: NIH RePORTER
Antigen-presenting cells (APCs) induce T cell activation as well as T cell tolerance. The molecular basis of the regulation of this critical 'decision' is not well understood. Here we show that HDAC11, a member of the HDAC histone deacetylase family with no prior defined physiological function, negatively regulated expression of the gene encoding interleukin 10 (IL-10) in APCs. Overexpression of HDAC11 inhibited IL-10 expression and induced inflammatory APCs that were able to prime naive T cells and restore the responsiveness of tolerant CD4(+) T cells. Conversely, disruption of HDAC11 in APCs led to upregulation of expression of the gene encoding IL-10 and impairment of antigen-specific T cell responses. Thus, HDAC11 represents a molecular target that influences immune activation versus immune tolerance, a critical 'decision' with substantial implications in autoimmunity, transplantation and cancer immunotherapy.
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