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).