Abstract
Normal intestinal mucosa contains abundant immunoglobulin A (IgA)-secreting cells, which are generated from B cells in gut-associated lymphoid tissues (GALT). We show that dendritic cells (DC) from GALT induce T cell-independent expression of IgA and gut-homing receptors on B cells. GALT-DC-derived retinoic acid (RA) alone conferred gut tropism but could not promote IgA secretion. However, RA potently synergized with GALT-DC-derived interleukin-6 (IL-6) or IL-5 to induce IgA secretion. Consequently, mice deficient in the RA precursor vitamin A lacked IgA-secreting cells in the small intestine. Thus, GALT-DC shape mucosal immunity by modulating B cell migration and effector activity through synergistically acting mediators.
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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B-Lymphocytes / immunology*
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B-Lymphocytes / metabolism
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Cell Movement
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Cells, Cultured
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Chemotaxis, Leukocyte
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Dendritic Cells / immunology*
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Immunity, Mucosal
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Immunoglobulin A / biosynthesis*
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Immunoglobulin A / immunology
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Interleukin-5 / immunology
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Interleukin-6 / immunology
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Intestinal Mucosa / immunology
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Intestines / cytology
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Intestines / immunology*
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Lymphoid Tissue / cytology
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Lymphoid Tissue / immunology
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Mice
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Mice, Inbred C57BL
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Receptors, Antigen, B-Cell / biosynthesis
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Tretinoin / immunology
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Vitamin A / physiology
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Vitamin A Deficiency / immunology
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Vitamins / immunology
Substances
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Immunoglobulin A
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Interleukin-5
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Interleukin-6
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Receptors, Antigen, B-Cell
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Vitamins
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Vitamin A
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Tretinoin