Distribution of Interferon-Gamma Receptors in Normal and Psoriatic Skin

• Published in: Pathology, research and practice Vol. 191; no. 6; pp. 530 - 534
• Main Authors: van den Oord, J.J., De Ley, M., De Wolf-Peeters, C.
• Format: Journal Article
• Language: English
• Published: Germany Elsevier GmbH 01.07.1995
• Subjects: Antigens, CD - analysis; Cytokine; Cytokine-receptor; HLA-DR Antigens - analysis; Humans; Immunohistochemistry; Intercellular Adhesion Molecule-1 - analysis; Interferon gamma Receptor; Psoriasis; Receptors, Interferon - analysis; Skin - chemistry; Cytokine-receptor; Immunohistochemistry; Cytokine
• ISSN: 0344-0338; 1618-0631
• DOI: 10.1016/S0344-0338(11)80872-1

Recent data suggest that imbalances in production and secretion of cytokines, in particular interferon-gamma (IFN-γ), may be crucial in the pathogenesis of psoriasis. In order to exert its role on target cells, IFN-γ has to interact with a specific cell membrane receptor termed the IFN-γ-receptor (IFN-γR). We studied the distribution of IFN-γRs in frozen skin biopsies from 25 psoriatics and 5 normal controls with two unrelated monoclonal antibodies, and compared its distribution with that of the IFN-γ-inducible HLADR- and ICAM-1 antigens. In normal skin, IFN-γRs were restricted to the basal cell layer; weak staining was found on scattered mononuclear cells in the papillary dermis. In 13/25 active Psoriatic lesions, additional suprabasal immunoreactive foci, and in 5/25 cases, diffuse immunoreactivity of the entire epidermis were seen. No striking topographical similarities between the site and number o f IFN-γR+, HLADR+ and ICAM-1 + keratinocyte foci were observed, suggesting that cytokines other than IFN-γ induce HLADR-antigens on Psoriatic keratinocytes in vivo. The restricted distribution o f IFN-γR on the germinative cell layer in normal skin confirms the role played by IFN-γ in the normal growth regulation o f the epidermis. The de novo suprabasal expression o f IFN-γR in psoriasis argues against the current hypothesis that IFN-γR are down-regulated due to a local excess o f IFN-γ or transforming growth factor alpha (TGF-α). Whether IFN-γRs in psoriatic skin are functionally normal and involved in signal transmission, remains to be studied.