Interleukin-4-dependent innate collaboration between iNKT cells and B-1B cells controls adaptative contact sensitivity
Interleukin-4-dependent innate collaboration between iNKT cells and B-1B cells controls adaptative contact sensitivity
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DOI：
10.1111/j.1365-2567.2006.02330.x
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发表时间：
2006-04-01
期刊：
影响因子：
6.4
通讯作者：
Askenase, PW
中科院分区：
文献类型：
--
作者：
Campos, RA;Szczepanik, M;Askenase, PW
We showed that hepatic V alpha 14(+) invariant natural killer T (iNKT) cells, via their rapid interleukin (IL)-4 production, activate B-1 cells to initiate contact sensitivity (CS). This innate collaboration was absent in IL-4(-/-) and signal transducer and activator of transcription (STAT)-6(-/-) mice and was inhibited by anti-IL-4 treatment. These mice have defective CS because they fail to locally recruit the sensitized effector T cells of acquired immunity. Their CS is reconstituted by transfer of downstream-acting 1-day immune B-1 cells from wild-type mice. Responses were not reconstituted with B-1 cells from IL-4 receptor-alpha(-/-) or STAT-6(-/-) mice, nor by IL-4 treatment of B cell-deficient mice at immunization. Finally, IL-4 was preferentially and transiently produced by hepatic iNKT cells within 7 min after sensitization to mediate collaboration between innate-like iNKT cells and the B-1 B cells that participate in the recruitment of effector T cells in vivo.
