Interleukin-4-dependent innate collaboration between iNKT cells and B-1B cells controls adaptative contact sensitivity

被引:28
作者
Campos, RA
Szczepanik, M
Itakura, A
Lisbonne, M
Dey, N
Leite-de-Moraes, MC
Askenase, PW
机构
[1] Yale Univ, Sch Med, Dept Internal Med, Allergy & Clin Immunol Sect, New Haven, CT 06520 USA
[2] Univ Hosp, Serv Prof Edgar Santos, Salvador, BA, Brazil
[3] Jagiellonian Univ, Coll Med, Dept Human Dev Biol, Krakow, Poland
[4] Univ Paris 05, Hop Necker Enfants Malad, UMR 8147, CNRS, Paris, France
关键词
B-1B cells; contact sensitivity; interleukin-4; signal transducer and activator of transcription-6; V alpha 14(+) natural killer T cells;
D O I
10.1111/j.1365-2567.2006.02330.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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.
引用
收藏
页码:536 / 547
页数:12
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