Innate and adaptive immunity cooperate flexibly to maintain host-microbiota mutualism.
Innate and adaptive immunity cooperate flexibly to maintain host-microbiota mutualism.
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先天和适应性免疫会灵活合作，以维持宿主 - 微生物互助。
DOI：
10.1126/science.1172747
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发表时间：
2009-07-31
期刊：
影响因子：
--
通讯作者：
Macpherson AJ
中科院分区：
文献类型：
--
作者：
Slack E;Hapfelmeier S;Stecher B;Velykoredko Y;Stoel M;Lawson MA;Geuking MB;Beutler B;Tedder TF;Hardt WD;Bercik P;Verdu EF;McCoy KD;Macpherson AJ
哺乳动物肠道下部的共生细菌数量是身体细胞的10倍。我们研究了不同免疫机制在限制肠道微生物群传播方面的相对重要性。在这里，我们揭示了先天性和适应性免疫功能之间的灵活连续体，包含肠道微生物。缺乏关键先天免疫功能（如Toll样受体信号传导或氧化爆发产生）的小鼠自发产生针对其肠道微生物群的高滴度血清抗体。这些抗体反应在先天性免疫缺陷时对维持体内宿主-宿主互惠共生具有重要的功能。继发于先天性免疫缺陷的针对肠道微生物群的适应性免疫的自发超活化可以阐明其中涉及免疫功能障碍的炎性疾病的潜在机制。
Commensal bacteria in the lower intestine of mammals are 10 times as numerous as the body’s cells. We investigated the relative importance of different immune mechanisms in limiting the spread of the intestinal microbiota. Here, we reveal a flexible continuum between innate and adaptive immune function in containing commensal microbes. Mice deficient in critical innate immune functions such as Toll-like receptor signaling or oxidative burst production spontaneously produce high-titer serum antibodies against their commensal microbiota. These antibody responses are functionally essential to maintain host-commensal mutualism in vivo in the face of innate immune deficiency. Spontaneous hyper-activation of adaptive immunity against the intestinal microbiota, secondary to innate immune deficiency, may clarify the underlying mechanisms of inflammatory diseases where immune dysfunction is implicated.
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