Stimulatory lipids accumulate in the @entity19 liver within 30 min of contact sensitization to facilitate the activation of Na  ve iNKT cells in a XXXX -dependent fashion.

@entity776 @entity5 @entity19 @entity5526 @entity56 @entity58 @entity1909
Natural killer T cells with invariant ab-T cell receptors (TCRs) (iNKT cells) constitute a lipid-responsive arm of the innate immune system that has been implicated in the regulation or promotion of various immune, infectious and @entity5 . @entity5526 ( @entity5526 ), also known as @entity56 or @entity56 contact @entity1909 , is one such immune process that begins with topical sensitization to an allergen and culminates in a localized cutaneous inflammatory response after challenge with the same allergen. @entity5526 depends on events initiated early in sensitization by hepatic iNKT cells. We have shown previously that these iNKT cells release @entity58 early after skin sensitization to activate B-1 B cells to produce IgM antibodies that aid in local recruitment of the effector T cells. Here, we utilize adoptive transfer techniques in several strains of knockout @entity19 to demonstrate that hepatic lipids isolated 30 min after sensitization are significantly more stimulatory to na  ve hepatic iNKT cells than hepatic lipids isolated after sham sensitization. These stimulatory hepatic lipids specifically affect iNKT cells and not B-1 B cells. The downstream @entity5526 response is abrogated with anti- @entity776 -blocking antibodies, suggesting a critical role of @entity776 in the activation of hepatic iNKT cells with these lipids. Hepatocytes may not be essential, as donor hepatic iNKT cells can reconstitute @entity5526 without migrating to the recipient @entity19 liver. Rather, @entity776 -expressing liver mononuclear cells are sufficient for activation of iNKT cells. In conclusion, stimulatory lipids accumulate in the liver soon after sensitization and facilitate iNKT cell activation in a @entity776 -dependent yet potentially hepatocyte-independent manner.
