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Prepublished online as a Blood First Edition Paper on November 14, 2002; DOI 10.1182/blood-2002-04-1230.
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Blood, 1 April 2003, Vol. 101, No. 7, pp. 2704-2710
IMMUNOBIOLOGY
Antigen presentation by mouse CD4+ T cells involving
acquired MHC class II:peptide complexes: another mechanism to limit
clonal expansion?
Julia Y. S. Tsang,
Jian Guo Chai, and
Robert Lechler
From the Department of Immunology, Division of
Medicine; and Transplantation Biology, Medical Research Council
Clinical Science Centre, Hammersmith Campus of Imperial College
Faculty of Medicine, London, United Kingdom.
Antigen presentation by activated human and rat CD4+ T
cells has long been known to induce hyporesponsiveness due to a
combination of anergy and apoptosis. It has been assumed that no such
phenomenon occurs in mice due to the inability of mouse T cells to
synthesize major histocompatibility complex (MHC) class II
molecules. There have been several recent descriptions of the transfer
of molecules, including MHC molecules, from antigen-presenting cells
(APCs) to T cells. Here, we describe the acquisition of MHC class II molecules by T-cell receptor (TCR)-transgenic T cells and
T-hybridoma cells following culture with APCs. Acquisition was markedly
enhanced by T-cell activation either due to cognate recognition of
antigen or anti-CD3 activation. When activation was induced by antigen recognition, preferential acquisition of complexes of class II molecules displaying cognate peptide was observed; in contrast, following activation by anti-CD3 the acquisition of class II molecules was MHC unrestricted. T cells that had acquired MHC class II:peptide complexes were able to act as APCs and induced proliferation and interleukin-2 secretion by resting T cells. However, when activated T
cells that had acquired MHC class II:peptide complexes engaged in T:T
interactions, this led to an increase in apoptosis and the induction of
hyporesponsiveness. These results raise the possibility that the
acquisition of MHC class II:peptide complexes by T cells during an
immune response may serve to limit clonal expansion, including that
induced by alloantigen following tissue or stem cell transplantation.
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