Abstract
We showed that hepatic Valpha14+ 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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adoptive Transfer
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Animals
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Antigens, Differentiation, B-Lymphocyte / analysis
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B-Lymphocyte Subsets / immunology*
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Cell Communication / immunology
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Dermatitis, Contact / etiology
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Dermatitis, Contact / immunology*
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Female
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Flow Cytometry
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Histocompatibility Antigens Class II / analysis
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Immune Tolerance / immunology
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Interleukin-4 / biosynthesis
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Interleukin-4 / immunology*
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Killer Cells, Natural / immunology*
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Liver / immunology
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Lymphocyte Activation / immunology
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Male
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Mice
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Mice, Inbred BALB C
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Mice, Inbred CBA
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Picryl Chloride
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Receptors, Antigen, T-Cell, alpha-beta / analysis
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Receptors, Interleukin-4 / immunology
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STAT6 Transcription Factor / immunology
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T-Lymphocyte Subsets / immunology*
Substances
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Antigens, Differentiation, B-Lymphocyte
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Histocompatibility Antigens Class II
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Receptors, Antigen, T-Cell, alpha-beta
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Receptors, Interleukin-4
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STAT6 Transcription Factor
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Stat6 protein, mouse
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invariant chain
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Interleukin-4
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Picryl Chloride