Oral mucosal immunity
Oral mucosal immunity
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DOI：
10.1016/j.oooo.2013.07.013
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发表时间：
2013-11-01
影响因子：
2.9
通讯作者：
Lemmer, J.
中科院分区：
文献类型：
--
作者：
Feller, L.;Altini, M.;Lemmer, J.
口腔粘膜的角质形成细胞和树突状细胞通过分子模式识别受体区分口腔和病原微生物，并介导对潜在入侵病原体的保护性免疫炎症反应的产生或介导对口腔微生物的免疫耐受。口腔免疫耐受是由于T细胞对抗原的免疫原性呈递缺乏应答或调节性T细胞抑制效应T细胞的活性所致。口腔粘膜部位分泌的免疫球蛋白A（sIgA）抗体通过限制微生物的定植及其对上皮的侵袭而有助于口腔免疫。IG同种型转换为伊加依赖于或不依赖于T辅助细胞，并由树突状细胞和单核细胞分泌的细胞因子促进。
Oral keratinocytes and dendritic cells of the oral mucosa, through molecular pattern recognition receptors, distinguish between commensal and pathogenic microorganisms and mediate the generation of protective immunoinflammatory responses to potentially invading pathogens or mediate immune tolerance toward commensal microorganisms. Oral immune tolerance is the result either of lack of activation of T cells in response to immunogenic presentation of antigens or of suppression of activity of effector T cells by regulatory T cells.Secretory immunoglobulin A (sIgA) antibodies at oral mucosal sites contribute to oral immunity by limiting colonization of microorganisms and their invasion of the epithelium. Ig isotype class switching to IgA is either dependent on or independent of T helper cells and is facilitated by cytokines secreted by dendritic cells and monocytes.