期刊
JOURNAL OF IMMUNOLOGY
卷 177, 期 10, 页码 6650-6659出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.10.6650
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资金
- Medical Research Council [G0400421] Funding Source: researchfish
- MRC [G0400421] Funding Source: UKRI
- Medical Research Council [G0400421] Funding Source: Medline
- NHLBI NIH HHS [R01 HL071590] Funding Source: Medline
- NIAID NIH HHS [R01-AI054451, K08-AI050601] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
Although invariant NKT (iNKT) cells participate in many aspects of immune responses, the molecular mechanisms regulating their development, maturation, and activation are still poorly understood. GATA-3 is a T cell-specific transcription factor that is also expressed in iNKT cells. The critical role of GATA-3 in conventional alpha beta T cells has been well documented, but whether GATA-3 also regulates the development and function of iNKT cells is unknown. In the present study, we report that deficiency of GATA-3 results in cell-intrinsic defects in the thymic development and peripheral maturation of murine iNKT cells. In addition, GATA-3 is also required for survival, activation, and effector functions of this unique population of T cells. Our data also reveal a previously unidentified peripheral maturation step that is GATA-3 dependent.
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