期刊
SCIENCE
卷 314, 期 5802, 页码 1157-1160出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1132742
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资金
- Medical Research Council [G9818340B] Funding Source: researchfish
- Medical Research Council [G0601816] Funding Source: Medline
- NHLBI NIH HHS [HL54936, HL56949, HL62524] Funding Source: Medline
- NIAID NIH HHS [R37 AI054636, AI-061663] Funding Source: Medline
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.
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