The epidermis has been increasingly identified as a place where immune responses can originate. Accordingly the epidermis harbors dendritic bone marrow derived cells with antigen presenting capacity [1] and recently in the murine system a Thy-1+ cell expressing T cell receptor y and ounits was detected [2]. Moreover, keratinocytes have been identified as immunocompetent cells by their capacity to release a variety of immunomodulatory cytokines upon stimulation [3](table 1).

Cytokines are glycoproteins which are synthesized as well as secreted by various cells and which bind to specific receptors on target cells. As more of these mediators were isolated, characterized and cloned, the evidence for a network of interacting mediators was increasing, which leads to activation, proliferation and differentiation of both immune and nonimmune cells, stimulation and differentiation of stem cells and regulation of nonspecific inflammatory reactions such as acute phase protein production and fever. Similar to other cytokines, these epidermal cell derived mediators originally were described according to their biological and biochemical characteristics. Recently, cloning of these factors provided formal evidence for their existence. Accordingly, murine keratinocytes following appropriate stimulation synthesize and release interleukin 1?(IL-1?), interleukin 1 (IL-1), interleukin 3 (IL-3), granulocyte-macrophage colony stimulating factor (GM-CSF) and transforming growth factor-(TGF), but not IL-2 and IL-4 [3]. Human keratinocytes and carcinoma cell lines are known to produce IL-1?, IL-1, IL-6, tumor necrosis factor-?(TNF?), GM-CSF, granulocyte-CSF (G-CSF) and macrophage-CSF (M-CSF,