Abstract
Recent studies have suggested that thymic stromal lymphopoietin (TSLP) activates LCs to induce the differentiation of naive T cells into Th2 cells, and previous documentations underscore the contributory role of TSLP in the pathogenesis of AD via this type of DCs. Meanwhile, TSLP receptor (TSLPR) is expressed on various immunocompetent cells, including mast cells, basophils, monocytes, and T cells, indicating the possibility of direct TSLP interaction with these cells. We therefore investigated the expression of TSLPR, focusing on T cells. In freshly isolated PBMCs from normal individuals, TSLPR expression was minimal (0.045% of PBMCs) while PBMCs from AD patients demonstrated increased frequencies of TSLPR+CD4+T cells (0.40% of PBMCs) (p < 0.05). TSLPR+ T cells were CCR4+, CXCR3−, CLA+, CCR7−, CCR10+, and CD45RO+, indicative of skin-homing effector CD4+ T cells. Furthermore, CD4+ T cells isolated from PBMCs of AD patients (n = 23) and normal individuals (n = 7) were stimulated with anti-CD3/28 Ab-coated microbeads with or without rhTSLP, and cultured for 48 h. Subsequently, supernatants were collected and cytokine concentration was measured by CBA assay. Production of IL-4 was enhanced by 30% in CD4+ T cells from AD patients in response to TSLP, and secretion of IL-17A also increased moderately (10%). In comparison, CD4+ T cells from normal individuals responded to TSLP with augmented production of IFN-g, but not with IL-4 or IL-17A. In conclusion, TSLP seems to possess the ability to directly modify the cytokine producing ability of effector T cells, and the effect was favored toward Th2 in AD. Interestingly, TSLP acted differently on T cells of normal individuals, and this discrepancy in the T cell response to TSLP may be associated with the development of AD.
Published Version
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