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Prepublished online as a Blood First Edition Paper on November 14, 2002; DOI 10.1182/blood-2002-04-1230.
Submitted May 3, 2002
Accepted November 6, 2002
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*
Department of Immunology, Hammersmith Campus, Imperial College of Science, Technology and Medicine, London, United Kingdom
Department of Transplantation Biology, MRC Clinical Science Center, ICSTM, London, United Kingdom
* Corresponding author; email: r.lechler{at}ic.ac.uk.
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 synthesise 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 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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