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Proposed ole oF HLA-GWe nthe pathogenes oT psoriasis, ‘Antigen (Kg) Inthe binding pocket of HLA-Cw8 interacts wih a T-cell ceptor. The role of HLA-Cu6 In ‘sorasis key fo be twobl. MLA-Ou6 Is active in ross-presentng peptides on Ie suface of Gena els, allowing actvaton ani cloral expansion of antiges-spesiic CD8+ Tcels. This process i dependent ‘on COd+ Teel help for coss-presetaion of inracelular enigens and ls Ikely © happen toth i the dermis (activation of memory resident T cels) and local lymph nodes (astvaton of naive T cel) ‘Subsequent, te CO- Teele ae ate 1 migrate into the epidermis where they enceurer HLA.CHE on the surtace ofthe Keratinocytes sresenting fase same pathegenic peples. Activated COB Tells may recagniza pepites presenied by HLA-CW8 on keratineyte call surface. Bacause these T.cels express perforin, they could drectly damage keratinocytes In the traditional eyletoxic manrer. Activated CD8* T Gels could ase toger the local release sluble factors. including cvickines, chemokines, etosaroids, andr inate immune mediates, which could furher increase lzal irfamnaton and. stimulate keratinocyte prolfeation. In response to elthe insult, Keratineytes could respond by elaborating autocrine growh faciors sich 25 TGF-a and AREG, thereby encouraging their own prolferaton and sual

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