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Enhanced Responses of Glycosylphosphatidylinositol Anchor-Deficient T Lymphocytes¹

Wouter L. W. Hazenbos^2,*, Yoshiko Murakami^*, Jun-ichi Nishimura, Junji Takeda and Taroh Kinoshita^3,*

^* Department of Immunoregulation, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; Division of Medical Oncology and Transplantation, Duke University Medical Center, Durham, NC; and Department of Social and Environmental Medicine, Osaka University Medical School, Osaka, Japan

The functions of GPI-anchored proteins in T lymphocyte activation have been controversial. This issue was addressed by studying the responses of T lymphocytes from T lymphocyte-specific GPI anchor-deficient mice to different stimuli that normally allow coligation of TCR and GPI-anchored proteins. Stimulation of GPI anchor-deficient T lymphocytes with ConA induced 2-fold higher proliferative responses than did normal cells. In response to allogeneic stimulation, proliferation of GPI anchor-deficient T lymphocytes was enhanced 2- to 3-fold. The response to ConA of a GPI anchor-deficient anti-OVA T lymphocyte clone generated from these mice was 3-fold higher than that of cells from the same clone in which GPI anchor expression was restored by retroviral transduction. The response of the GPI anchor-deficient cloned anti-OVA T lymphocytes to antigenic stimulation was similar to that of the retrovirally restored cells. These results indicate that coligation with GPI-anchored proteins counteracts the response to TCR stimulation by ConA or alloantigen but not protein Ag.