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Immunoregulation in Epidermis: Glucocorticoids Induced Epidermal Cell Derived Inhibitor of Interleukin 1 Activity

  • M. L. Lukić
  • S. Stošić-Grujičić
  • Dj. Lalošević
  • S. Vukmanović
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 237)

Abstract

Epidermis, in addition to being a surface barrier, actively participates in various immunologic and inflammatory reactions in the skin. It is already well established that dendritic cells within epidermis such as Langerhans cells may function as antigen presenting cells and thereby play an important role during the initiation of an immune response (1). Among immunologically active elements resident in the epidermis the major cell population is the keratinocytes. They are able to produce several nonspecific immunoregulatory mediators including an immunoenhancing cytokine — epidermal cell (EC) derived thymocyte activating factor — which is indistinguishable from macrophage — derived interleukin 1 (IL 1) (reviewed in 2). We have analyzed recently the accessory cell function of mouse and human epidermal cells (ECs) by measuring their capacity to support the proliferative response of lectin-stimulated nonadherent thymic T cells (NATs)(3). NATs exhibit low responsiveness to lectins, while the addition of ECs induced in a dose-dependent way either supportive or suppressive effects. Having in mind that functional capacity of epidermal cells can be altered by various physico-chemical agents we have analysed the effects of glucocorticoids on the accessory function of epidermal cells. We present here evidence that in vivo exposure of ECs to glucocorticoids not only inhibits the production of IL 1 but also favors the production of factors which suppress NAT proliferation. Additionally we have shown the existence of an immunoinhibitory factor(s) produced by ECs which represent(s) an inhibitor of IL 1 — activity.

Keywords

Epidermal Cell Triamcinolone Acetonide Accessory Function Human Epidermal Cell Steroid Preparation 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1988

Authors and Affiliations

  • M. L. Lukić
    • 1
    • 2
  • S. Stošić-Grujičić
    • 1
    • 2
  • Dj. Lalošević
    • 1
    • 2
  • S. Vukmanović
    • 1
    • 2
  1. 1.Institute for Biological ResearchUniversity of BelgradeBelgradeYugoslavia
  2. 2.Institute of Microbiology and ImmunologySchool of MedicineYugoslavia

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