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ePaper created 2014-09-15, 12:31:02 | version 1.32.01
The Skin Immune System The first immunohistological studies in psoriatic skin demonstrated the importance of T lymphocytes and their subsets in psoriasis.[1] This understanding coincided with the discovery of monoclonal antibodies for detection of new T-cell subsets. At the same time, the T-cell selective immunosuppressant cyclosporine was successfully introduced for the treatment of psoriasis, underlining the pivotal role of activated T cells in this skin disease. All these developments led to the concept of the skin immune system that was published in 1986.[2] The term “skin immune system - SIS” was introduced to underline the complexity of cells and mediators present in normal human skin (resident) and those that invade it during different inflam- matory and immune-mediated skin diseases (recruited). Thereby, a more complete approach to normal human skin and its inflammatory and autoimmune diseases was promoted. For example, in psoriasis, which was regarded as a disease of keratinocyte hyperproliferation and granulocyte infiltration, it was found that different subsets of T cells might also play a role. The subsequent findings that T-cell inhibitors such as cyclosporin and the biologics directed against T cells were very effective, further endorsed the view that psoriasis might well be an autoimmune, T-cell-mediated disease. A similar situation occurred in understanding atopic dermatitis. The received idea was that it was a disease related to the other manifestations of atopy, rhinitis and asthma. A primary role was given to mast cells and their mediators, as well as to the IgE molecules on their membranes. By carefully immunophenotyping the subpopulation of inflammatory cells, it could not be denied that T cells were prominent in the superficial layers of atopic skin. And again, the T-cell inhibitor cyclosporin proved to be very effective, also in severe cases.[2,3,4] In the late nineties, the “millennium criteria” for atopic dermatitis were introduced, distinguishing between atopic dermatitis and so-called atopiform dermatitis.[5] This discussion and the criteria for atopic dermatitis have yet to be concluded. References 1. Bos JD, Hulsebosch HJ, Krieg SR, et al. Immuncompetent cells in psoriasis; in situ immunophenotyping by monoclonal antibodies. Arch Dermatol Res 1983; 275: 181-9. 2. Bos JD, Kapsenberg ML. The Skin Immune System (SIS): its cellular constituents and their interactions. Immunology Today 1986; 7: 235-40. 3. Bos JD, editor. Skin Immune System (SIS). CRC Press, Inc. Boca Raton, Flo, USA. ISBN 0-8493 4945-1. 4. Bos JD, Rie MA de. The pathogenesis of psoriasis : immunological facts and speculations. Immunol Today 1999; 20: 40-6. 5. Bos JD. Atopiform dermatitis. Br J Dermatol 2002; 147: 415-7. 36 BWEADVSMGFINCORR:Opmaak 1 21-07-2014 17:39 Pagina 36