期刊
NATURE IMMUNOLOGY
卷 18, 期 11, 页码 1249-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3837
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资金
- University of Alabama at Birmingham (UAB)
- National Institutes of Health [1R01 AI110480, R01 AI116584, AI097357, AI109962, AIAI109962, AI061061, AI049360]
- National Center for Research Resources, National Institutes of Health [1 G20RR022807-01]
- [P30 AR048311]
- [P30 AI027767]
Interleukin 2 (IL-2) promotes Foxp(3+) regulatory T (T-reg) cell responses, but inhibits T follicular helper (T-FH) cell development. However, it is not clear how IL-2 affects T follicular regulatory (T-FR) cells, a cell type with properties of both T-reg and TFH cells. Using an influenza infection model, we found that high IL-2 concentrations at the peak of the infection prevented TFR cell development by a Blimp-1-dependent mechanism. However, once the immune response resolved, some T-reg cells downregulated CD25, upregulated Bcl-6 and differentiated into T-FR cells, which then migrated into the B cell follicles to prevent the expansion of self-reactive B cell clones. Thus, unlike its effects on conventional T-reg cells, IL-2 inhibits T-FR cell responses.
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