Prens E, t Hooft-Benne K, Tank B, Van Damme J, van Joost T, Benner R
Department of Immunology, Erasmus University Rotterdam, The Netherlands.
Arch Dermatol Res. 1996 Feb;288(2):68-73. doi: 10.1007/BF02505046.
Membrane molecules such as CD36 (OKM5), intercellular adhesion molecule-1 (ICAM-1, CD54), gamma interferon-induced protein 10 (gamma-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 samples from all patients by mAb to CD2 (LFA-2), CD11a (LFA-1alpha), CD18 (LFA-1beta), ICAM-1, CD58 (LFA-3) and an antiserum to IL-1beta. 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-1beta in the MECLR emphasizes its relevance in psoriasis.
膜分子如CD36（OKM5）、细胞间黏附分子-1（ICAM-1，CD54）、γ干扰素诱导蛋白10（γ-IP10）和白细胞介素-1在银屑病表皮中被诱导和/或上调。这些分子在免疫系统中具有重要的辅助、运输或信号传导功能，并且在银屑病的病理生理学中也起作用。在体外自体混合表皮细胞-T淋巴细胞反应（MECLR）中研究了黏附分子、CD36和表皮白细胞介素-1在银屑病中的相关性。通过阻断特异性单克隆抗体和抗血清或在MECLR之前从表皮细胞悬液（ECS）中去除CD36+细胞，对银屑病患者表皮细胞悬液中它们的表达水平进行定量，并评估其功能。银屑病皮损的ECS中CD36+（23±12%）、ICAM-1(+)（31±14%）和IL-1(+)（57±21%）细胞数量增加。所有患者样本中的自体MECLR均被抗CD2（淋巴细胞功能相关抗原2，LFA-2）、抗CD11a（淋巴细胞功能相关抗原1α，LFA-1α）、抗CD18（淋巴细胞功能相关抗原1β，LFA-1β）、抗ICAM-1、抗CD58（淋巴细胞功能相关抗原3，LFA-3）单克隆抗体和抗白细胞介素-1β抗血清抑制。因此，黏附分子不仅通过在银屑病皮损中黏附和募集T淋巴细胞促进炎症，还通过激活T细胞促进炎症。此外，银屑病表皮细胞上的CD36分子在银屑病中不协同刺激自体T淋巴细胞。在MECLR中观察到的白细胞介素-1β的协同刺激功能强调了其在银屑病中的相关性。
