Abstract
LPS stimulated B-1 cell polyclonal in vivo IgM responses depend on IL-4 release by invariant Valpha14+Jalpha18+ NKT (iNKT) cells. The IgM Abs can recruit effector T cells to mediate contact sensitivity. LPS activates the B-1 cell response just 1 day later, and depends on CD1d, iNKT cells, IL-4, TLR4, and MyD88. LPS in vivo and in vitro stimulates rapid preferential production of IL-4 in hepatic iNKT cells within 2 h. TLR4 were demonstrated in iNKT cells by flow cytometry and functional studies. Thus, innate microbial stimulation via TLR can activate iNKT cell and B-1 cell collaboration. The result is polyclonal IgM Ab responses capable of recruiting Ag-specific T cells into tissues. This may be involved in the promotion of autoimmunity by infectious agents.
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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Animals
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Antigens, CD1 / metabolism
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Antigens, CD1d
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B-Lymphocytes / immunology
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Immunity, Innate
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Immunoglobulin M / biosynthesis
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In Vitro Techniques
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Interleukin-4 / biosynthesis*
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Killer Cells, Natural / immunology*
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Lipopolysaccharides / pharmacology
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Lymphocyte Activation / drug effects
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Lymphocyte Cooperation / drug effects
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Male
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Mice
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Mice, Inbred BALB C
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Mice, Inbred C3H
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Mice, Inbred C57BL
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Mice, Inbred CBA
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Mice, Knockout
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T-Lymphocyte Subsets / immunology*
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Toll-Like Receptor 4 / deficiency
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Toll-Like Receptor 4 / genetics
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Toll-Like Receptor 4 / metabolism*
Substances
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Antigens, CD1
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Antigens, CD1d
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Immunoglobulin M
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Lipopolysaccharides
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Tlr4 protein, mouse
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Toll-Like Receptor 4
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Interleukin-4