Interleukin-4 therapy of psoriasis induces Th2 responses and improves human autoimmune disease - PubMed (original) (raw)

doi: 10.1038/nm804. Epub 2002 Dec 2.

Peter Thomas, Susanne Breit, Martin Dugas, Reinhard Mailhammer, Willem van Eden, Ruurd van der Zee, Tilo Biedermann, Jörg Prinz, Matthias Mack, Ulrich Mrowietz, Enno Christophers, Detlef Schlöndorff, Gerd Plewig, Christian A Sander, Martin Röcken

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Interleukin-4 therapy of psoriasis induces Th2 responses and improves human autoimmune disease

Kamran Ghoreschi et al. Nat Med. 2003 Jan.

Abstract

Selective skewing of autoreactive interferon-gamma (IFN-gamma)-producing T helper cells (Th1) toward an interleukin-4 (IL-4)-producing (Th2) phenotype can in experimental animals alleviate autoimmune disease without inducing general immunosuppression. In a prospective dose escalation study, we assessed treatment with human IL-4 (rhuIL-4) in 20 patients with severe psoriasis. The therapy was well tolerated, and within six weeks all patients showed decreased clinical scores and 15 improved more than 68%. Stable reduction of clinical scores was significantly better at 0.2-0.5 microg rhuIL-4 than at < or =0.1 microg rhuIL-4 (P = 0.009). In psoriatic lesions, treatment with 0.2-0.5 microg/kg rhuIL-4 reduced the concentrations of IL-8 and IL-19, two cytokines directly involved in psoriasis; the number of chemokine receptor CCR5+ Th1 cells; and the IFN-gamma/IL-4 ratio. In the circulation, 0.2-0.5 microg/kg rhuIL-4 increased the number of IL-4+CD4+ T cells two- to three-fold. Thus, IL-4 therapy can induce Th2 differentiation in human CD4+ T cells and has promise as a potential treatment for psoriasis, a prototypic Th1-associated autoimmune disease.

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