Regulation of the immune system skin effect.docVIP

 PAGE \* MERGEFORMAT 8 Regulation of the immune system skin effect Figure 1: normal skin and inflammatory skin conditions, skin cells, Langerhans cells and T cell interactions. Phenomenon of a long plagued scientists - UV light can inhibit the skin’s immune response - finally get a scientific explanation. Light and a number of other incentives by promoting skin cell RANKL (receptor activator of NF-κ B ligand) expression, to promote regulatory T cells (regulatory T cells, Tregs) proliferation. The skin is always exposed to environmental stimulation under such circumstances, they may cause an imbalance in the body’s immune system. For example, when exposed to ultraviolet light under the skin, the immune system is suppressed: ultraviolet light can be part of the treatment of psoriasis (psoriasis) - an autoimmune disease. Now, Loser for us to find a clue to explain why some environmental stimulus, such as ultraviolet light caused by certain skin inflammation, inhibit local and systemic immune response 〔 1〕 . They sketched out a cellular and molecular dynamic maps, activated inflammation of the skin revealed epidermal keratinocytes (keratinocyte), caused by regulatory T cells (Tregs) selective proliferation (preferential expansion); regulatory T cells can inhibit the skin and other tissue physiological and pathological immune response in a class of cells. Tregs, precisely, is the naturally occurring CD25 CD4 Tregs (see Note 1), can-specific expression of transcription factor Foxp3, the maintenance of the immune system self-tolerance (self tolerance), and inhibit the disorder or excessive immune response, such as self - immune diseases and allergy (Allergy), etc. 〔 2〕 . Interleukin -2 (Interleukin-2; IL-2) is a natural Tregs (natural Tregs) in peripheral immune system (peripheral immune system) essential for cell survival factor; CD25 (IL-2 receptor α chain) The same is also indispensable, and it involved constitutes a high affinity for IL-2 receptor 〔 3〕 . Inde