1. Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado, U.S.A.;
2. ^*Department of Pathology and Clinical Immunology, The University of Texas South-western Medical Center, Dallas, Texas, U.S.A.

Correspondence: Dr Donald Y.M. Leung, National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206

Received 30 June 1998; Revised 20 October 1998; Accepted 29 October 1998.

Abstract

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 to 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 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 skewing within the CLA⁺ subsets of both their CD4⁺ and their CD8⁺ T cells. T cell receptor V 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.