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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]

These include safeguarding cells against oxidative damage, facilitating amino acid transport, detoxifying foreign compounds, maintaining protein sulfhydryl groups in a reduced state, and acting as a cofactor for numerous enzymes

Future studies may help to further prove if it is safe and effective for larger groups of people