Evidence for superantigen involvement in skin homing of T cells in atopic dermatitis
Evidence for superantigen involvement in skin homing of T cells in atopic dermatitis
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DOI：
10.1046/j.1523-1747.1999.00502.x
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发表时间：
1999-02-01
影响因子：
6.5
通讯作者：
Leung, DYM
中科院分区：
文献类型：
--
作者：
Strickland, I;Hauk, PJ;Leung, DYM
The environmental factors that contribute to the homing of T cells in skin disease is unknown. The skin lesions of atopic dermatitis (AD) are frequently colonized with superantigen (SAg), producing strains of Staphylococcus aureus. In vitro, these superantigens have the capacity to activate and expand T cells expressing specific T cell receptor BV gene segments, and also to increase their skin homing capacity via upregulation of the skin homing receptor, cutaneous lymphocyte-associated antigen (CLA). These activities have been proposed Co enhance the chronic cutaneous inflammation of AD,but an in vivo role for SAg has not been conclusively demonstrated. In this study, we sought direct evidence for in vivo SAg activity by comparing the SAg profiles of S. aureus cultured from the skin of AD subjects to the T cell receptor V beta repertoire of their skin homing (CLA(+)) T cells in peripheral blood. SAg secreting S. aureus strains were identified in six of 12 AD patients, and all of these subjects manifested significant SAg-appropriate V beta skewing within the CLA(+) subsets of both their CD4(+) and their CD8(+) T cells. T cell receptor V beta skewing was not detectable among the overall CD4(+) or CD8(+) T cell subsets of these subjects, and was not present within the CLA(+) T cell subsets of five patients with plaque psoriasis and 10 normal controls. T cell receptor BV genes from the presumptively SAg-expanded populations of skin homing T cells were cloned and sequenced from three subjects and, consistent with a SAg-driven effect, were found to be polyclonal, We conclude that SAg can contribute to AD pathogenesis by increasing the frequency of memory T cells able to migrate to and be activated within AD lesions.
