
Glycosylphosphatidylinositol (GPI)‐anchored surface antigens in the allogeneic activation of T cells *
Author(s) -
SCHUBERT J.,
STROEHMANN A.,
SCHOLZ C.,
SCHMIDT R. E.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb06656.x
Subject(s) - immunology , t cell , stimulation , biology , antigen , cytokine , receptor , t lymphocyte , cd3 , microbiology and biotechnology , immune system , cd8 , endocrinology , genetics
SUMMARY GPI‐linked surface molecules have recently been described as structures with an activation potential for human T lymphocytes. To study the role of these molecules in T cell activation we analysed GPI‐deficient or normal T cells from patients with paroxysmal nocturnal haemoglobinuria (PNH). On activation with allogeneic Epstein‐Barr virus (EBV)‐transformed B cell lines GPI‐deficient freshly separated T cells or continuously growing T cell lines exhibited a significantly lower proliferation or cytokine production compared with their normal counterparts. In contrast, stimulation via the T cell receptor‐associated CD3 structure resulted in a comparable response. There was no difference in activation of normal T lymphocytes when GPI‐deficient B cells were used as stimulators compared with normal B cells obtained from the same PNH patient. We conclude from these data that GPI deficiency in PNH leads to a functional deficiency of GPI‐deficient T cells. In contrast, no difference in activation of T lymphocytes for GPI‐deficient cells on the stimulator cell level was observed.