TSLPR signals via JAK2 and NLRP3
It has been recently demonstrated that the development of EAE requires NLRP3 8. As we found above that TSLPR deficiency results in reduced CD4+ T lymphocytes infiltration in EAE development, we determined to examine whether TSLPR signaling requires NLRP3 inflammasome activation in EAE. Results showed that MOG35-55 treatment resulted in increased phosphorylation of JAK2 and expression of NLRP3 when compared to that in control mice (Fig 2A). Immunohistochemistry analysis of brain tissues fromTslpr +/+ and Tslpr-/- mice showed that MOG35-55 injection led to remarkable increase in NLRP3+ cells in the brain inTslpr+/+ mice when compared to that without MOG35-55 injection while a significant reduction in NLRP3+ cells was observed in brain tissue ofTslpr-/- mice when compared to that inTslpr+/+ mice after EAE induction (Fig 2B).