التفاصيل البيبلوغرافية
| العنوان: |
Deficiency of IL-22 Contributes to a Chronic Inflammatory Disease: Pathogenetic Mechanisms in Acne Inversa. |
| المؤلفون: |
Wolk, Kerstin1,2, Warszawska, Katarzyna1, Hoeflich, Conny3, Witte, Ellen1, Schneider-Burrus, Sylke4, Witte, Katrin1, Kunz, Stefanie1, Buss, Annette1, Roewert, Hans Joachim, Krause, Markus4, Lukowsky, Ansgar4, Volk, Hans-Dieter3, Sterry, Wolfram4, Sabat, Robert1,2 robert.sabat@charite.de |
| المصدر: |
Journal of Immunology. 1/15/2011, Vol. 186 Issue 2, p1228-1239. 12p. |
| مصطلحات موضوعية: |
*T cells, *CYTOKINES, *CARRIER proteins, *SKIN inflammation, *INFLAMMATION, *EPIDERMIS |
| مستخلص: |
Overexpression of the T cell cytokine IL-22 is linked to the development of some chronic diseases, but little is known about IL-22 deficiency in humans. As demonstrated in this study, acne inversa (AI; also designated as Hidradenitis suppurativa) lesions show a relative deficiency of IL-22 and IL-20, but not of IL-17A, IL-26, IFN-γ, IL-24, or IL-1β. Moreover, AI lesions had reduced expression of membranous IL-22 and IL-20 receptors and increased expression of the natural IL-22 inhibitor, IL-22 binding protein. AI is a chronic inflammatory skin disease with prevalence up to 4% of the population and in which cutaneous bacterial persistence represents an important pathogenetic factor. Accordingly, we also found a relative deficiency of antimicrobial proteins (AMPs) in AI lesions and a positive correlation between lesional IL-22 and IL-20 versus AMP levels. IL-22, like its tissue cell downstream mediator IL-20, upregulated AMPs in reconstituted human epidermis and was critical for increased AMP levels under inflammatory conditions. The relative IL-22 deficiency in AI was not linked to lesional T cell numbers or Th22/Th1/Th17 subset markers and -inducing cytokines. However, IL-10 was highly expressed in AI lesions and correlated negatively with IL-22 expression. Moreover, IL-10 inhibited IL-22 but not IL-17 production in vitro. The IL-10 overexpression, in turn, was not associated with an elevated presence of regulatory T cells but with the enhanced presence of an IL-10-inducing cytokine. We conclude that IL-22 deficiency may contribute to the pathogenesis of certain chronic disorders as postulated in this paper for AI. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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