Mallon E, Young D, Bunce M, Gotch F M, Easterbrook P J, Newson R, Bunker C B
Department of Dermatology, Imperial College School of Medicine, Chelsea and Westminster Hospital, London SW10 9NH, U.K.
Br J Dermatol. 1998 Sep;139(3):527-33. doi: 10.1046/j.1365-2133.1998.02495.x.
The aetiopathogenesis of psoriasis is unknown, but genetic and environmental factors may be involved. Psoriasis may not be one disease but a cutaneous inflammatory reaction pattern consequent upon several different independent or related stimuli in susceptible individuals. There are controversial issues regarding the immunological basis of psoriasis and the role of CD4 vs. CD8 T lymphocytes. Psoriasis has been associated with HLA-Cw6 and Cw7 by serology and specifically with HLA-Cw0602 by polymerase chain reaction (PCR) typing. Psoriasis is probably no more common in HIV infection than in the general population; however, it may appear for the first time or pre-existing psoriasis may worsen and be difficult to treat in HIV disease. We have investigated the prevalence of HLA-C alleles, in the specific clinical context of HIV infection complicated by type 1 psoriasis, in a case control study of 14 men with HIV disease and type 1 psoriasis and 147 HIV-infected patients without psoriasis. Typing was performed using PCR with sequence-specific amplification primers. Eleven of 14 patients (79%) with psoriasis carried the HLA-Cw0602 allele compared with 24.5% of those without psoriasis (odds ratio = 11.31; 95% confidence limits 2. 73 to 65.36; P = 0.0001). Two patients without the HLA-Cw0602 allele carried instead the closely related Cw0401/3 allele. The results confirm the previously reported association between the HLA-Cw0602 allele and type 1 psoriasis, and suggest that the association with HLA-Cw0602 is stronger in HIV-associated psoriasis although this trend needs to be supported by a larger sample. The immunodysregulation resulting from HIV infection may trigger psoriasis in those genetically predisposed by the Cw*0602 allele. As CD8 T cells recognize antigens in the context of class I major histocompatibility complex, the identification of an HLA class I association in HIV-associated psoriasis strengthens the argument for an important role for CD8 + T lymphocytes in the immunopathogenesis of psoriasis. Investigations of the pathogenesis of psoriasis should take account of clinical and other subtypes already identified.
银屑病的发病机制尚不清楚,但可能涉及遗传和环境因素。银屑病可能并非单一疾病,而是易感个体在受到几种不同的独立或相关刺激后产生的一种皮肤炎症反应模式。关于银屑病的免疫学基础以及CD4与CD8 T淋巴细胞的作用,存在一些有争议的问题。通过血清学研究发现银屑病与HLA - Cw6和Cw7相关,通过聚合酶链反应(PCR)分型则明确与HLA - Cw0602相关。银屑病在HIV感染者中的发病率可能并不高于普通人群;然而,银屑病可能首次出现,或者既往存在的银屑病可能会加重,且在HIV疾病中难以治疗。我们在一项病例对照研究中,调查了14例患有HIV疾病且伴有1型银屑病的男性患者以及147例未患银屑病的HIV感染者中,HLA - C等位基因的频率。采用序列特异性扩增引物的PCR方法进行分型。14例银屑病患者中有11例(79%)携带HLA - Cw0602等位基因,而未患银屑病的患者中这一比例为24.5%(优势比 = 11.31;95%置信区间为2.73至65.36;P = 0.0001)。2例未携带HLA - Cw0602等位基因的患者携带的是与之密切相关的Cw0401/3等位基因。结果证实了先前报道的HLA - Cw0602等位基因与1型银屑病之间的关联,并表明在HIV相关银屑病中,与HLA - Cw0602的关联更强,尽管这一趋势需要更大样本的支持。HIV感染导致的免疫失调可能会在那些携带Cw*0602等位基因的遗传易感个体中引发银屑病。由于CD8 T细胞在I类主要组织相容性复合体的背景下识别抗原,在HIV相关银屑病中发现HLA I类关联,进一步支持了CD8 + T淋巴细胞在银屑病免疫发病机制中起重要作用的观点。银屑病发病机制的研究应考虑已确定的临床及其他亚型。