Langerhans Cells Suppress @entity71545 + NK Cell-Mediated XXXX .

@entity71545 @entity32 @entity19 @entity5132 @entity281 @entity777 @entity71544 @entity5350
Recruitment of innate immune effector cells into sites of @entity281 is a critical component of resistance to pathogen @entity281 . Using a model of intradermal footpad injection of @entity5132 , we observed that @entity32 as measured by footpad thickness and neutrophil recruitment occurred independent of adoptive immunity but was significantly reduced in MyD88(-/-) and @entity777 (-/-) @entity19 . Unexpectedly, huLangerin-DTA @entity19 (  LC) that lack Langerhans cells (LC) developed @entity32 and expressed higher amounts of @entity777 , suggesting a suppressive role for LC. Increased @entity32 also occurred in @entity5350 (-/-)   LC @entity19 but was reversed by Ab-mediated ablation of NK cells. @entity71544 (+) @entity71545 (+) NK cells are a liver-resident subset that can mediate inflammatory skin responses. We found that exaggerated @entity32 was absent in   LC * @entity71544 (-/-) @entity19 . Moreover, the exaggerated response in   LC @entity19 could be adoptively transferred with liver @entity71545 (+) NK cells. Finally, @entity71545 (+) NK cells in   LC but not control @entity19 were recruited to the skin, and inhibition of their recruitment prevented the exaggerated response. Thus, in the absence of LC, @entity71545 (+) liver NK cells display an inappropriately proinflammatory phenotype that results in @entity32 . These data reveal a novel function for LC in the regulation of this recently described subset of skin tropic NK cells.
