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Regulation of human T‐cell homing receptor expression in cutaneous bacterial infection
Author(s) -
Sieling Peter A.,
Legaspi Annaliza,
Ochoa Maria Teresa,
Rea Thomas H.,
Modlin Robert L.
Publication year - 2007
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2006.02528.x
Subject(s) - mycobacterium leprae , antigen , homing (biology) , lepromatous leprosy , immunology , tuberculoid leprosy , t cell receptor , biology , leprosy , t cell , receptor , lymphocyte homing receptor , t lymphocyte , microbiology and biotechnology , immune system , cell , ecology , biochemistry , cell adhesion , genetics
Summary We investigated the regulation of T‐cell homing receptors in infectious disease by evaluating the cutaneous lymphocyte antigen (CLA) in human leprosy. We found that CLA‐positive cells were enriched in the infectious lesions associated with restricting the growth of the pathogen Mycobacterium leprae , as assessed by the clinical course of infection. Moreover, CLA expression on T cells isolated from the peripheral blood of antigen‐responsive tuberculoid leprosy patients increased in the presence of M. leprae (2·4‐fold median increase; range 0·8–6·1, n = 17), but not in unresponsive lepromatous leprosy patients (1·0‐fold median increase; range 0·1–2·2, n = 10; P < 0·005). Mycobacterium leprae specifically up‐regulated the skin homing receptor, CLA, but not α 4 /β 7 , the intestinal homing receptor, which decreased on T cells of patients with tuberculoid leprosy after antigen stimulation (2·2‐fold median decrease; range 1·6–3·4, n = 3). Our data indicate that CLA expression is regulated during the course of leprosy infection and suggest that T‐cell responsiveness to a microbial antigen directs antigen‐specific T cells to the site of infection.