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

RA Campos, M Szczepanik, A Itakura… - …, 2006 - Wiley Online Library
RA Campos, M Szczepanik, A Itakura, M Lisbonne, N Dey, MC Leite‐de‐Moraes
Immunology, 2006Wiley Online Library
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 …
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.
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