Interleukin-4-dependent innate collaboration between iNKT cells and B-1 B cells controls adaptative contact sensitivity
Version of Record online: 14 MAR 2006
Volume 117, Issue 4, pages 536–547, April 2006
How to Cite
Campos, R. A., Szczepanik, M., Itakura, A., Lisbonne, M., Dey, N., Leite-de-Moraes, M. C. and Askenase, P. W. (2006), Interleukin-4-dependent innate collaboration between iNKT cells and B-1 B cells controls adaptative contact sensitivity. Immunology, 117: 536–547. doi: 10.1111/j.1365-2567.2006.02330.x
- Issue online: 14 MAR 2006
- Version of Record online: 14 MAR 2006
- Received 31 August 2005; revised 12 December 2005; accepted 15 December 2005.
- B-1 B cells;
- contact sensitivity;
- signal transducer and activator of transcription-6;
- Vα14+ natural killer T cells
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.