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One hypothesis for RA pathogenesis is that the disease begins in genetically predisposed individuals at mucosal sites (i.e., oral cavity, lung, gut) as a consequence of the interaction between a dysbiotic microbiota and the mucosal immune system, and then transitions to synovitis [8]

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PMID: 91 ZhangJWangYFanMGuanYZhangWHuangFet al

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Molecular mechanism of nrf2 activation by oxidative stress

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