Abstract

Psoriasis vulgaris (PV) is a skin disease present in 1–3% of the Caucasoid population [1]. Although genetic, immunological and environmental factors foster PV, there is evidence that immune system activation plays a central role in keratinocyte hyperproliferation, a typical feature of psoriasis. Moreover, actively dividing T cells accumulate in psoriatic lesions, apart from the presence of a variety of other antigen-presenting, effector and inflammatory cells in psoriatic skin [2]. Peptide presentation by MHC class II molecules is important in human autoimmune diseases. Most of these autoimmune diseases are genetically linked to particular alleles of the class II molecules, and much sequence information has also accumulated on the polymorphisms in these genes. In some autoimmune diseases almost all of the patients carry particular alleles of MHC class II genes (e.g. pemphigus vulgaris). In other autoimmune diseases several different MHC class II alleles carry increased risk, presumably because different MHC class II molecules present the relevant peptide(s) to T cells [3]. Studies have shown psoriasis susceptibity loci on chromosomes as follows: 1, 2, 3, 4, 6th, 8th, 16, 17, 19 and 20. As seen with most autoimmune diseases, psoriasis is found on 6p and associated with allelic component of the major histocompatibility complex [4]. HLA antigens are analysed in different populations and PV has been associated with several HLA class I and class II specifities [5–9]. Among these class I phenotypes Cw6 and B57 have been most consistently reported. The alleles corresponding to these phenotypes are in linkage disequilibrium in normal individuals and compose the proximal class I end of an ancestral haplotype called EH57.1. The class II side of EH57.1 ancestral haplotype contains DRB1* 07 and some other DRB1 alleles [10]. Studies suggest several genetic backgrounds for PV [11]. The first choice is that more than one allele at a single locus may confer susceptibility. The second is that alleles at more than one locus within the HLA region may also confer susceptibility. The true disease locus could be linked to, but separate from, one or more known HLA genes. Although present HLA association information tends to support the last-mentioned hypothesis, it does not in fact rule out the first two. A close linkage between HLA class III and PV has been reported in an Indian population [12]. This study investigates HLA-DRB1 association with PV in a Turkish population.

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