Five major functional pathways in pathogenesis of ReA
I, The deceased ratio of Th1/Th17 and increased myeloid cells caused by Chlamydia inflammation lead to the transmission of Chlamydia antigen [27,28]. II, Chlamydia-induced reactive arthritis is TNF-dependent inflammatory disease. Increased TNF-α production and deficient Treg control promoted ReA [14]. III, iNKT cells play a protective role against Salmonella-induced ReA by down-regulating IL17-γδT cells [26]. IV, Lactobacillus casei can inhibit the expression of TNF-α, IL-17, IL-23, IL-1 and IL-6 in intestinal lymph nodes which lead to protective role in ReA. V, TNFRp55 regulates the cytokine production and enhanced the production of IFN-γ and IL-17, which developed severe chronic Yersinia enterocolitica-induced (ReA) [32–34]. Note: Th1/Th17:Helper T cell; iNKT cell: Constant-type natural killer cell; υδT cell: Innate immune cell; TNF-RP55: TNF receptor of p55; (-): inhibition; (+): activation.”