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Interleukin‐4‐dependent innate collaboration between iNKT cells and B‐1 B cells controls adaptative contact sensitivity
Author(s) -
Campos Regis A.,
Szczepanik Marian,
Itakura Atsuko,
Lisbonne Mariette,
Dey Neelendu,
LeitedeMoraes Maria C.,
Askenase Philip W.
Publication year - 2006
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2006.02330.x
Subject(s) - innate immune system , natural killer t cell , biology , interleukin 12 , effector , immunology , microbiology and biotechnology , interleukin 4 , stat protein , immune system , signal transduction , in vitro , t cell , stat3 , cytotoxic t cell , biochemistry
Summary We showed that hepatic Vα14 + 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‐α –/– 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 .