Vol. 103 - No. 3 MINERVA MEDICA 183 cells is well characterized. 4, 5 Recent studies have focused on some key cytokines pro- duced by type 17 helper T (Th17) and type 1 helper T (Th1) cells which are responsible for infammation and proliferation of kerati- nocytes in psoriasis. 4 A common etiology for both psoriasis and autoimmunity is likely because, partic- ular types of autoantibodies are shown with psoriasis patients in many studies 6 and also in our previous study published in 2005, 7 but no reproducible autoantigen has yet been clearly defned. 8 Coexistence of pso- riasis with other autoimmune diseases has been reported in the literature and psoriasis is probably best placed within a group of autoimmune-related diseases characterized by chronic infammation in the absence of known infectious agents or antigens. 9 Serum IgA levels are increased or dec- reased in psoriasis 10 and circulating im- mune complexes have also been reported to be increased. 11 Anti-IgA antibodies are found in about 10% of patients with IgA defciency and with common variable im- munodefciency. There is a causal relation- ship between IgG-anti-IgA antibodies and the development of anaphylactoid reactions 1 Department of Pediatric Immunology Ege University Medical School, Izmir, Turkey 2 Department of Dermatology Ege University Medical School, Izmir, Turkey MINERVA MED 2012;103:183-7 E. AZARSIZ 1 , I. ERTAM 2 , N. KARACA 1 , G. AKSU 1 , S. ALPER 2 , N. KUTUKCULER 1 IgG-anti-IgA antibodies: an autoimmune fnding in patients with psoriasis vulgaris Aim. Psoriasis is thought to be an autoim- mune disease caused by inappropriate acti- vation of the cellular immune system. In this study, we aimed to search out IgG-anti-IgA antibody levels, serum immunoglobulins and antinuclear antibodies (ANA). Methods. The study entrolled 38 psoriasis vulgaris patients and 40 healthy controls. Results. Mean IgG-anti-IgA levels were sig- nifcantly higher in psoriasis patients. The frequency of positive ANA testing was 21.1%; however, there was no correlation between IgG-anti-IgA antibody levels and ANA positiv- ity. Only one patient had low IgA levels with- out high IgG-anti-IgA concentrations. Conclusion. The data about high IgG-anti- IgA antibody levels are noteworthy for a new evidence of autoimmune mechanism. Key words: Antibodies, anti-nuclear - Autoim- mune diseases - Psoriasis. P soriasis is a common chronic infam- matory disease of the skin and joints that affects approximately 2% of the global population. 1 Pathogenesis is not completely clear but today it is thought that psoriasis is the most prevalent autoimmune disease caused by inappropriate activation of the cellular immune system. 2, 3 Alterations in the innate and acquired immunologic sys- tem have been reported and hyperprolifera- tion of keratinocytes which is triggered by T Corresponding author: E. Azarsiz, MD,Ege Department of Pediatric Immunology, University Medical School, 35100- Izmir, Turkey.e-mail: elif.azarsiz@ege.edu.tr MINERVA MEDICA COPYRIGHT® This document is protected by international copyright laws. No additional reproduction is authorized. It is permitted for personal use to download and save only one file and print only one copy of this Article. It is not permitted to make additional copies (either sporadically or systematically, either printed or electronic) of the Article for any purpose. It is not permitted to distribute the electronic copy of the article through online internet and/or intranet file sharing systems, electronic mailing or any other means which may allow access to the Article. The use of all or any part of the Article for any Commercial Use is not permitted. The creation of derivative works from the Article is not permitted. The production of reprints for personal or commercial use is not permitted. It is not permitted to remove, cover, overlay, obscure, block, or change any copyright notices or terms of use which the Publisher may post on the Article. It is not permitted to frame or use framing techniques to enclose any trademark, logo, or other proprietary information of the Publisher.