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Psoriasis patients generate increased serum levels of autoantibodies to tumor necrosis factor-α and interferon-α

R. BergmanaCorresponding Author Informationemail address, M. Ramona, G. Wildbaumb, E. Avitan-Hersha, E. Mayera, A. Shemerc, N. Karinb

Received 9 June 2009; received in revised form 25 August 2009; accepted 29 August 2009. published online 12 July 2010.
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Abstract 

Background

It has been shown in experimental animal models that were extended to humans that during autoimmune conditions, the immune system generates beneficial autoantibody (auto Ab) response to a limited number of inflammatory mediators that drive the pathogenesis of the disease.

Objective

To investigate the presence of auto Abs to cytokines and chemokines in psoriasis.

Methods

Sera were obtained from patients with psoriasis (n=37), atopic dermatitis (AD) (n=18) and healthy volunteers (n=56). The titers of auto (Abs) to TNF-α, interferon-α (IFN-α), interleukin-17 (IL-17), and chemokines CCL2, CCL3 and CCL5 were determined using enzyme-linked immunosorbant assay. Neutralizing activities of high-titer auto Abs to TNF-α and IFN-α were determined using functional in vitro assays.

Results

Highly significant increased titers of auto Abs to TNF-α and IFN-α were detected in patients with psoriasis compared with healthy subjects and patients with AD (mean titers more than fourfold). These auto Abs demonstrated some neutralizing activity in vitro, but their serum levels did not correlate with the intensity and duration of the disease and with phototherapy induced remissions. Significantly increased titers albeit to a lesser extent, of auto Abs to CCL3 were detected in AD.

Conclusions

Psoriasis patients produce markedly increased levels of auto Abs to TNF-α and IFN-α which are two of the key cytokines in this disorder. The presence of these auto Abs which possess some neutralizing activity in vitro, may be an epiphenomenon or might play a role in attempting to suppress the ongoing inflammatory process.

a Department of Dermatology, Rambam Medical Center, Israel

b Department of Immunology and The Bruce Rappaport Faculty of Medicine, and the Rappaport Family Institute for Research in the Medical Sciences ,Haifa, Israel

c Department of Dermatology, Sheba Medical Center, Tel-Aviv, Israel

Corresponding Author InformationCorresponding author at: Department of Dermatology, Rambam Medical Center, POB 9160, Haifa, 31096, Israel. Tel.: +972 4 8542610; fax: +972 4 8542951.

PII: S0923-1811(09)00261-8

doi:10.1016/j.jdermsci.2009.08.006