Double-stranded RNA induces melanocyte death via activation of XXXX .

@entity1 @entity6800 @entity66 @entity3963 @entity1800 @entity2391 @entity7375 @entity30462 @entity1366 @entity10886
As cutaneous pigment-producing cells, melanocytes can become targets of primary and secondary immune response as can be seen in @entity66 and @entity7375 . @entity1800 have previously been implicated as a possible precipitating factor in the destruction of melanocytes in these disorders. During viral replication, double-stranded RNA (dsRNA) is produced as an intermediate metabolite, which induces antiviral and inflammatory responses through @entity6800 ( @entity6800 ) in cells of innate immune system. The functional responses of melanocytes to dsRNA, however, remain unclear. Herein, we demonstrated that @entity1 melanocytes expressed @entity6800 at a constitutive and inducible level. Stimulation with poly(I:C), a synthetic dsRNA analogue, triggered apoptosis of melanocytes. The apoptosis-inducing effect was shown by RNA interference to be largely dependent on @entity6800 , but occurred independently of NF-kB activation since treatment with specific NF-kB inhibitor @entity30462 failed to prevent the process. In contrast, @entity2391 neutralizing Ab blocked the apoptosis-inducing effect of dsRNA, indicating the involvement of @entity2391 autocrine signalling. Furthermore, studies on the intracellular signal transduction pathways revealed that dsRNA induces the activation of @entity3963 , @entity1366 and @entity10886 in melanocytes. Using specific inhibitors, we demonstrated that activation of @entity3963 and @entity1366 controlled both @entity2391 secretion and @entity2391 mediated cell death. Taken together, these data suggest that viral dsRNA stimulates @entity6800 in @entity1 melanocytes and triggers the cellular apoptosis through autocrine of @entity2391 .
