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Errol Prens Klazina't Hooft-Benne Bhupendra Tank Jozef Van Damme Theodoor van Joost Robbert Benner 《Archives of dermatological research》1996,288(2):68-73
Membrane molecules such as CD36 (OKM5), intercellular adhesion molecule-1 (ICAM-1, CD54), gamma interferon-induced protein
10 (γ-IP10) and IL-1 are induced and/or upregulated in psoriatic epidermis. These molecules have important accessory, trafficking
or signalling functions in the immune system and also play a role in the pathophysiology of psoriasis. The relevance of adhesion
molecules, CD36 and epidermal IL-1 in psoriasis was studied in vitro in the autologous mixed epidermal cell-T lymphocyte reaction
(MECLR). Their level of expression was quantitated in epidermal cell suspensions (ECS) from patients with psoriasis and their
function was assessed by blocking with specific mAbs and antisera or by depleting CD36+ cells from the ECS prior to the MECLR. ECS from psoriatic lesions contained increased numbers of CD36+ (23±12%), ICAM-1+ (31±14%) and IL-1+ (57±21%) cells. The autologous MECLR was inhibited in saaples from all patients by mAb to CD2 (LFA-2), CD11a (LFA-1α), CD18
(LFA-1β), ICAM-1, CD58 (LFA-3) and an antiserum to IL-1β. Thus, adhesion molecules facilitate inflammation in psoriasis not
only via adhesion and recruitment of T lymphocyte in psoriatic lesions, but also via activation of T cells. Furthermore CD36
molecules on psoriatic epidermal cells do not costimulate autologous T lymphocytes in psoriasis. The observed costimulatory
function of IL-1β in the MECLR emphasizes its relevance in psoriasis. 相似文献
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