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Antigen‐driven shedding of L‐selectin from human γδ T cells
Author(s) -
SANCHEZGARCIA J.,
ATKINS C.,
PASVOL G.,
WILKINSON R. J.,
COLSTON M. J.
Publication year - 1996
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1996.d01-729.x
Subject(s) - antigen , biology , stimulation , t cell receptor , t lymphocyte , l selectin , t cell , immunology , population , gamma delta t cell , polyclonal b cell response , microbiology and biotechnology , antigen presenting cell , cell adhesion molecule , immune system , medicine , endocrinology , environmental health
Activation of lymphocytes leads to the modulation of a number of surface molecules. We have investigated the expression of one such molecule, L‐selectin, following activation of γδ T cells with Mycobacterium tuberculosis . L‐selectin is modulated during lymphocyte entry into lymph nodes; this modulation reflects the recirculation and homing potential of lymphocytes. We find that stimulation of γδ T cells by M. tuberculosis antigens results in shedding of L‐selectin from γδ T cells. Re‐expression of L‐selectin occurs on removal of antigen suggesting that the regulation of expression is controlled by the presence or absence of antigen. The γδ T‐cell receptor (TCR)‐positive, L‐selectin negative population of peripheral blood lymphocytes appears to be resting cells, as assessed by forward‐ and light‐scatter analysis. We further find that γδ T cells isolated from a site of infection, the pleural fluid of a tuberculosis patient, are L‐selectin negative, and that L‐selectin is re‐expressed following culture of the pleural fluid γδ T cells in the absence of antigen. These results demonstrate that, in addition to stimulation with polyclonal mitogens, antigen stimulation can also promote the surface shedding of L‐selectin and that γδ T cells have the potential to home to sites of infection supporting their role in the immunological defence against infectious micro‐organisms.