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Effector and regulatory T cells derived from the same T cell clone differ in MHC class II‐peptide multimer binding
Author(s) -
Nolte‘t Hoen Esther N. M.,
Amoroso Maria Grazia,
Veenstra Jetty,
GrosfeldStulemeyer Mayken C.,
van Eden Willem,
Broeren Chris P. M.,
Wauben Marca H. M.
Publication year - 2004
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.200425563
Subject(s) - biology , t cell , mhc class ii , microbiology and biotechnology , mhc restriction , cytotoxic t cell , major histocompatibility complex , t cell receptor , peptide , effector , mhc class i , antigen , immunology , biochemistry , immune system , in vitro
Abstract MHC class II‐peptide multimers are a valuable tool for antigen‐specific detection of CD4 + T cells. However, it has been proposed that T cells in a hypo‐responsive state can have diminished binding of such multimers. In the present study, we investigated this phenomenon at the clonal level. We found that anergic CD4 + T cells had a reduced capacity to bind MHC class II‐peptide multimers compared to their non‐anergic counterparts. Increasing the incubation temperature, time, or MHC‐peptide valency could not equalize multimer binding by anergic and non‐anergic T cells. Neither anergic T cells nor non‐anergic T cells internalized the MHC class II‐peptide dimers efficiently, and in both cases the dimers bound to the plasma membrane at locations containing a low amount of raft‐associated lipids. Disruption of lipid rafts, however, led to decreased dimer binding by non‐anergic T cells and to a lesser extent by anergic T cells. Finally, we show that the depth of the anergic state of the T cell, which determines its ability to regulate other T cell responses, correlates with the reduced dimer binding. We here demonstrate for the first time differential MHC class II‐peptide multimer binding by regulatory (anergic) and effector T cells with identical TCR.