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J Invest Dermatol. 1994 Feb;102(2):145-9.

T cells involved in psoriasis vulgaris belong to the Th1 subset.

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  • 1First Department of Medicine, University of Mainz, Germany.


Although the pathogenesis of psoriasis vulgaris is still unknown, several characteristics point to an immunologically mediated process. Epidermal psoriatic lesions are characterized by a hyperproliferation of keratinocytes and an infiltration of T lymphocytes and granulocytes. Because the former may be mediated in part by lymphokines secreted by T cells, we have focused our interest on the in vivo and in vitro cytokine secretion patterns of T lymphocytes from psoriatic lesions. In five patients T lymphocytes were obtained from epidermal specimens. The cells were propagated with lectin and irradiated feeder cells and subsequently cloned by limiting dilution. The resulting T-cell clones were phenotypically and functionally characterized. Our data show that the majority of T-cell clones were CD4+ (74%), whereas only 25% were CD8+ and 1% were CD4-/CD8-. Also, we have further investigated the cytokine secretion pattern of T-cell lines or CD4+ T-cell clones, respectively. All cells tested produced interferon-gamma whereas only a minority secreted interleukin (IL)-4. Moreover, these cells produced high amounts of IL-2 but only little or no IL-10 or tumor necrosis factor-alpha. To correlate these data with the in vivo situation, biopsies from psoriatic lesions of five patients were investigated for the presence of the mRNA of IL-4, IL-10, and interferon-gamma using the polymerase chain reaction. In these biopsies only the mRNA for the Th1 cytokine interferon-gamma but not for the Th2 cytokines IL-4 and IL-10 could be detected. Identical experiments were performed to test the in vivo cytokine production of synovial fluid mononuclear cells of two patients with arthropathia psoriatica. Again, only the mRNA for interferon-gamma but not IL-4 could be detected. This indicates that T cells involved in psoriasis exhibit a Th1-like cytokine secretion profile.

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