@entity14293 -mediated @entity1569 -like XXXX is dependent on @entity636 .

@entity16821 @entity14293 @entity1569 @entity19 @entity1373 @entity164 @entity2169 @entity636
@entity14293 and Th17 cells producing @entity636 and @entity16821 are found in excess in skin affected by @entity1569 . Previous studies showed that @entity16821 , but not @entity636 , mediates @entity1569 -like @entity1373 following recombinant @entity19 (rm) @entity14293 injections into skin. To further investigate the role of @entity636 , ears of @entity19 were injected with rmIL-23. Investigators blinded to treatment conditions and @entity19 genotypes measured @entity2169 , epidermal thickness, and cytokine expression. In @entity164 ( @entity164 ) @entity19 , rmIL-23 induced @entity2169 (p < 0.001, all p values versus saline), @entity1373 by histology (p < 0.001) and confocal microscopy (p < 0.004), and expression of both @entity636 and @entity16821 . As expected, rmIL-23 injections into @entity16821 (-/-) @entity19 resulted in relatively @entity2169 (p < 0.09) and @entity1373 (p < 0.51 by histology and p < 0.75 by confocal microscopy). Notably, rmIL-23 injections into @entity636 (-/-) @entity19 produced @entity2169 (p < 0.001, versus @entity14293 -injected @entity164 @entity19 ) and @entity1373 (p < 0.001 by histology and p < 0.005 by confocal microscopy), even though @entity16821 was readily induced in these @entity19 . Furthermore, systemic delivery of blocking Abs directed against either @entity16821 or @entity636 completely inhibited @entity14293 -induced @entity1373 in @entity164 @entity19 . These results demonstrate that @entity636 , like @entity16821 , is a downstream mediator for @entity14293 -induced changes in @entity19 skin and that both of these Th17 cytokines are necessary to produce @entity14293 -mediated skin pathology. @entity636 may represent an attractive therapeutic target in individuals with @entity1569 by blocking downstream effects of @entity14293 .
