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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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A significantly greater proportion of Hispanic patients had LT in the post-MMAT era, likely reflecting efforts across the country to mitigate access disparities

rNAPRT, as previously observed for eNAMPT (132, 146, 148), is also able to force monocyte differentiation into macrophages, up-regulating macrophage colony-stimulating factor (M-CFS)