The Expression And Significanceof Of Interleukin-5 And Interleukin-17 In The Patients With Bullous Pemphigoid

Object: Detection of bullous pemphigoid in lesion tissue of patients with IL-5and IL-17expression, and to investigate the effect of IL-5and IL-17 in bullous pemphigoid occurs in thedevelopment of the mechanism of action and the clinical significance.Methods: The SABC immunchistochemical technique was used to test the expression ofIL-5 and IL-17 in 38 Bullous Pemphigoid lesions and 20 normal skins.Results:. Bullous pemphigoid lesions in the positive expression of IL-5 are mainlydistributed in the epidermal layer especially to the basilar membrane, the positive expression ofIL-17 distributed in the epidermal layer; and in normal skin tissues are called negative or weaklypositive expression. Both in bullous pemphigoid in lesional and normal skin tissue expressiondifferences were statistically significant ( IL-5: t= - 14.617, P < 0.05; IL-17: t= - 23.756; P <0.05 ), bullous pemphigoid lesions in IL-5 and IL-17 expression levels were positively correlated( r = 0.842, P < 0.05 )[1].Conclusion:①Of bullous pemphigoid lesions in patients with IL-5、IL-17 expressionwater average increased, suggesting that both in bullous pemphigoid lesions formationdevelopment may play an important role in.②In bullous pemphigoid patients increased IL-5expression possible mechanism is: In bullous pemphigoid disease process, eosinophils are themajor components of the inflammatory response. IL-5 is only produced by the Th2 cells, it is inTh2 cells plays an important role, because IL-5 is Th2 feature of the cell factor, the role of thecharacteristic, such as proliferation, differentiation, chemotaxis and IL-5 are closely linked. Inbullous pemphigoid patients, IL-5and eosinophil chemotactic factors work together to promoteeosinophil transendothelial basal layer mobile, stimulate superoxide anion release, while IL-5andeosinophil chemotactic factors also promote eosinophilic granules in the cytoplasm of release[2、3],and IL-5 can release various proteases and inflammatory mediators, eventually leading tobullous pemphigoid lesions formation.③Bullous pemphigoid patients increased IL-17expression was the likely mechanism of cytokine secretion: Th17 through IL-17, IL-22, IL-21,IL-10, IL-6, etc, these cytokines induced by the interaction of or directly resulted in bullouspemphigoid patients with inflammatory reaction and tissue damage, some cytokines and the roleof promoting IL-17 cell secretion, leading to bullous pemphigoid disease exacerbations. IL-6isone of many autoimmune diseases is an important cytokine. IL-6 can stimulate B lymphsubstantial differentiation, resulting in a large number of autoantibodies, while IL-6 also can induce T lymphoid proliferation, into cytotoxic lymphocyte. According to the above research, itcan be speculated that, IL-6 is to promote T, B lymphocyte transformation in important inducer,and T, B lymphocytes autoimmune disease is important in cell, this shows IL-6 may inautoimmune disease -- bullous pemphigoid play a key role. Th17 secretion of pro-inflammatorycytokines, such as IL-22, TNF-α, these strong inflammatory factor may be the cause of ourclinical see on skin erythema, ulceration is one of the reasons[3]。④IL-5and IL-17 in bullouspemphigoid expression was positively related to the occurrence and the development of，themechanism is not clear, the author speculation : possible mechanism for Th17 cells, IL-5 andTh17 cells secreting many cytokines, their interaction, mutual influence, promote, inducedbullous pemphigoid, advance jointly pemphigus in response to inflammation and tissue injury ofmucosa development.