Th-17 cell activation in response to high salt following @entity810 is associated with progressive @entity82 and attenuated by XXXX antagonism.

@entity8 @entity82 @entity7940 @entity63 @entity11264 @entity1809 @entity1808 @entity1372 @entity740 @entity9886 @entity810 @entity35 @entity3457
Exposure of @entity35 to elevated dietary salt following recovery from @entity810 ( @entity810 ) accelerates the transition to @entity740 ( @entity740 ), and is dependent on lymphocyte activity. Here we tested whether high salt diet triggers lymphocyte activation in @entity8 and @entity82 . Male @entity35 on a 0.4% salt diet were subjected to left unilateral @entity63 -reperfusion and allowed to recover for 5 weeks. This resulted in a mild elevation of @entity11264 (+) T cells relative to sham animals. Contralateral unilateral nephrectomy and elevated dietary salt (4%) for 4 extra weeks hastened @entity740 and @entity82 . @entity3457 cells were increased in the kidney threefold after 4 weeks of elevated dietary salt exposure relative to post- @entity810 @entity35 before salt feeding. The T cell subset was largely positive for @entity7940 , indicative of Th-17 cells. Because @entity1808 activity may influence lymphocyte activation, injured @entity35 were given the @entity1809 antagonist, @entity9886 , along with high salt diet. This significantly reduced the number of renal Th-17 cells to levels of sham @entity35 , and significantly reduced the salt-induced increase in @entity82 to about half. In vitro studies in @entity810 -primed @entity11264 (+) T cells indicated that @entity1808 and extracellular @entity1372 enhanced, and @entity9886 inhibited, @entity7940 expression. Thus, dietary salt modulates immune cell activity in postischemic recovering kidneys because of the activity of local RAS, suggesting the participation of these cells in @entity740 progression post- @entity810 .
