Clinical Features And The Effect Of Th17 In Atopic Dermatitis

Atopic dermatitis (AD) is a chronic, recurrent, itching and inflammatory skin disease. It usually presents from early infancy, and may continue several years even to adulthood. Its incidence has increased in the past three decades , with children rising from 10% to 20% and adult from 1% to 3% [1]. Atopic dermatitis is seasonal to some degree and differs in sexes, races and regions.The course of AD involves many factors, including environment, society, economic status, psychological condition, living habit and infection etc. It also has complex clinical features, including concomitant diseases, concomitant symptoms and different degree of skin damage in different clinical stages. Based on allergy evidences, Wuthrich [2] divided AD into two different subtype, intrinsic atopic dermatitis (IAD) and extrinsic atopic dermatitis(EAD). We usually need to verify allergens as well as the severity of the state of illness by clinical diagnosis, including prick skin tests and general serum IgE levels, so as to distinguish the from the two subtypes, and eventually to guide treatment.With unclear etiopathogenisis and complex pathogenesy, AD has always been considered as a polygenic disease, involving the interaction in environment, gene and immune system. Many etiological factors contribute to the onset of AD, and factors related to our research are immune function abnormity, the disbalance of Th1/Th2 and autoimmune phenomena Autoimmune phenomena is one of the factors related closely to our research, and detected circulative IgE to human self-protein and immune complex of autoantigen and IgE were observed in many patients with AD. And some researchers reported that that the autoantigen was intra-cellular antigen [3]. In addition, some reports showed that some patients with AD had antinuclear antibody (ANA), and the patients with AD accompanied with facial rash trend to have positive symptom of ANA [4]. The above-mentioned phenomenon suggests the following reaction mechanism: foreign antigens stimulates organism to produce IgE, and then the antigen-IgE complex induce histoclasia and exposed autoantigen. Autoantigen-autoantibody complex was formed and presented. And eventually megacell and eosinophile granulocyte were activated to release cytokines to aggravate histoclasia. It formed a bad recycle and a persistent and (or) severe inflammatory reaction, even when breaking away from sensitization surroundings [5].The discovery of new Th17 cells caused people doubt about the the role of Th17 in the onset mechanism of AD . In 2003, Toda [6] first reported that the expression of IL-17 involved in the damage of AD, and subsequent researched came then. In 2008, Koga [7] found that Th17 cells occurs in the peripheral blood and skin damage, and he also found its quantity relate with the severity of AD.Our research separates into two parts, investigation and experiment. Sixty patients with AD, consistent with the Hanifin and Rajka criteria, from the clinic service of Institute of Dermatology of Chinese PLA, Xijing Hospital, Fourth Military Medical University, from the November 2007 to the Janurary 2009, were included in our study.We found the following clinical features different from previous reports: Distinguished from foreign reports that the season deviation of AD often occurred in winter, we found it occurred in summer and winter, especially in summer; 35% of patients suffered from season and temperature factors simultaneously; no vocational factor was found; xerodermia and allergic rhinitis was the most common symptoms and the most common disease accompanied with AD respectively. We also found that one patient and three others with their relatives had psoriasis; allergic rhinitis is the most common family history distinguished from asthma reported by previous reseachers. The research also showed that 31.67% of patients had negative skin prick test, paprika and egg were the most common food allergen, 66.67% of the patients had normal general IgE. We analyzed clinical features and laboratory data simultaneously, and then discovered the following phenomena: 35% of patients had positive SPT and normal general IgE, 33.33% of patients had positive SPT and elevated general IgE, and 31.67% of patients had negative SPT and normal general IgE. We divided them into two subtypes, 20 patients belonging to EAD and 19 patients to IAD. The other 21 patients had more complex clinical features, and we supposed that the patients with atopic disease belonged to EAD and the patients without atopic disease belonged to IAD.We had to detect specific IgE and ask more detailed history to make definite diagnosis and discrimination.Objective: To investigate the correlation between the pathogenesy of AD and Th17 cells, to identify the elevated cell factors related with Th17cells in the patients serum with AD, to further verify the role of Th17 cells in the course of AD, and make a new direction on its therapeutics.Methods: We used case control study for the investigation. We collected non-blood relation patients with AD and hospitalized patients of congenital heart disease or postburn scar, and then extract serum from their peripheral blood. We used ELISA to detect cell factors related with Th17cells(IL-17, IL-21,IL-22,IL-23), and then to compare their disparation.T test was used in group comparison, and Pearson correlation analysis was used in dependability analysis.Results: T tests showed significant differences in IL-17, IL-22 and IL-23 between the two groups by (p<0.05), with the case group higher than the control, while the IL-21 showed difference between the two groups, but without statistical significance (p>0.05). Pearson correlation analysis showed significant correlation between each other (p<0.05) except IL-21 and IL-22. T tests also showed almost no statistical significance (p>0.05) in clinical subgroups of AD, such as in the light, middle and heavy, or between EAD and IAD, or between normal and abnormal general IgE.Conclusion: The cell factors related with Th17 cells occured in the course of AD, which provide evidence for the function of Th17 in the pathogenesy and course of AD. IL-17, the most important cell factor for the biological effect of Th17, plays an important role.It can raise neutrophil and promote release of inflammatory cell factors to aggravate the patient's condition of AD. And it can stimulate epithelial cell and fibroblast to release inflammatory cell factors to remodel the skin structure of AD. Now many biologic agents are being developed in the world, such as IL-17R fusion protein and anti-IL-17 antibody which were made as targeted drugs to effect IL-17 and IL-17R. Therefore if we can further indentify the function of Th17 to AD, we can attempt to use the biologic agents to improve the state of inflammation and to relieve the condition of illness.