Targeting CD8+ T cells prevents psoriasis development

Protective and pathogenic roles of resident memory T cells in human skin disorders

“…Going back to the first engrafted mouse model, it can be presumed that CD69 + CD8 T cells in the engrafted skin originated from the skin T RM that have existed in the non-lesional psoriatic skin from the beginning. Furthermore, this psoriatic disease formation in the grafted skin was prevented by neutralizing CD8 [30]. These results demonstrate that skin CD8 T RM , especially epidermal CD8 T RM , play an inevitable role in the lesion formation of psoriasis.…”

Targeting L-type amino acid transporter 1 in innate and adaptive T cells efficiently controls skin inflammation

“…8,10 Although the increased frequency of gd T cells has been observed also in human psoriatic lesions, 2 their relevance in the onset or recurrence of disease is not clearly established. 43,44 Indeed, human psoriatic lesions show a greater frequency of IL-17-releasing TCRab 1 T cells than gd T cells. 32 Our data demonstrate that LAT1 deletion in CD4 T cells dampens IMQ-induced skin inflammation.…”

Psoriasis: a mixed autoimmune and autoinflammatory disease

“…A large proportion of CD8+ T cells in psoriatic lesions are oligoclonal[9] suggesting that these cells have expanded as a response to a limited set of antigens. These cells produce pathogenic IL-17, a key driver of psoriasis inflammation[10,11], and neutralization of CD8+ T cells[12] or inhibition of T cell trafficking into the epidermis[13] prevents development of psoriasis in a xenograft model. These observations suggest that CD8+ T cells may be engaged in pathogenic crosstalk with keratinocytes through HLA-Cw*0602 and that this process is the central driver of inflammatory activity in chronic plaque psoriasis [12] (Figure 3).…”