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T helper 1 to T helper 2 shift in cytokine expression: an autoregulatory process in superantigen-associated psoriasis progression?

¹ Department of Microbiology, University College of Medical Sciences and Guru Teg Bahadur Hospital, Dilshad Garden, Delhi 110095, India

² Department of Dermatology and Venereal Disease, University College of Medical Sciences and Guru Teg Bahadur Hospital, Dilshad Garden, Delhi 110095, India

Correspondence
Sarika Jain
drsarikajn{at}yahoo.co.in

Received May 31, 2008
Accepted September 30, 2008

Psoriasis is an inflammatory skin disorder characterized by increased activation of CD4⁺ T lymphocytes, and systemic and local overexpression of pro-inflammatory cytokines such as interleukin 2 (IL-2), gamma interferon (IFN-), IL-6 and tumour necrosis factor alpha, indicating that immunopathogenesis of the disease is T helper 1 (Th1) mediated. Several studies suggest a pivotal role of bacterial superantigens in the initiation and/or exacerbation of this illness. This study was conducted to assess the systemic Th1/Th2 imbalance in Indian psoriasis patients presenting with variable duration of disease by studying systemic superantigen-stimulated peripheral blood mononuclear cell (PBMC) cytokine expression. PBMCs were isolated and stimulated in vitro with superantigens (streptococcal pyrogenic exotoxin A and staphylococcal enterotoxin B), and the cytokines released (IFN- for a Th1 response, and IL-4 and IL-10 for a Th2 response) were assayed. In contrast to controls, psoriasis patients in the early course of disease were characterized by significantly increased expression of the pro-inflammatory cytokine IFN-, whilst a shift towards IL-10 secretion (Th2 response) was observed in those presenting with increased duration of disease. These observations suggest a possible shift from a Th1 to a Th2 cytokine response with superantigen-associated progression for the duration of psoriasis, perhaps as an adaptive process by the immune system in an attempt to downregulate abnormal inflammatory Th1 immune responses.

Abbreviations: IFN-, gamma interferon; IL, interleukin; PBMC, peripheral blood mononuclear cell; PHA, phytohaemagglutinin; PV, psoriasis vulgaris; SEB, staphylococcal enterotoxin B; SPEA, streptococcal pyrogenic exotoxin A; Th, T helper.