Abstract

Abstract CPPs is characterized by hyperproliferation of keratinocytes (KC) and T-cell (Tc)/DCs activation. IL-32, which induces TNF and activates NFkB and p38 MAPK, is involved in early inflammation. We investigated the role of IL-32 in the pathogenesis of CPPs by IHC, ECL and qRT-PCR analysis. Biopsy tissues were obtained from CPPs patients with active disease (N=20) and healthy human controls (N=15). A mouse Mab against human IL-32 and mouse IgG1 isotype antibody were used. IHC staining of IL-32 was performed on deparaffinized sections of formalin-fixed tissues by an indirect imunoperoxidase method (EnVision, Dako). IL-32 was expressed in basal KC with cytoplasmic granular staining. IL-32 was also expressed in DCs with strong nuclear and cytoplasmic staining in dermis. IL-32 was weakly expressed in the nucleus of KC in healthy human skin. Induction of IL-32 was detected in human KC lysates after stimulation with TNF and IL-1 or cell contact with activated Tc, but not in KC supernatants, indicating IL-32 is not secreted from KC in vitro. ECL/qRT-PCR results showed IL-32 and other CPPs-relevant cytokines (IL-18, IL-20, 22 and 23) were significantly (P<0.05) increased. Our data support the hypothesis that IL-32 is a novel proinflammatory cytokine which is involved in the pathogenesis of CPPs, especially in epidermal regions of the skin where innate immune mechanisms are central to host defense.

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