Glycosylphosphatidylinositol (GPI)-anchored surface antigens in the allogeneic activation of T cells.
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.
Schubert
J
J
Department of Medicine, Hannover Medical School, Germany.
Stroehmann
A
A
Scholz
C
C
Schmidt
R E
RE
D000954:Antigens, Surface / Q000502:physiology*; D001402:B-Lymphocytes / Q000502:physiology; D017261:Glycosylphosphatidylinositols / Q000172:deficiency / Q000502:physiology*; D006457:Hemoglobinuria, Paroxysmal / Q000276:immunology*; D004854:Herpesvirus 4, Human; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis; D008213:Lymphocyte Activation; D013601:T-Lymphocytes / Q000276:immunology*
D000954:Antigens, Surface; D017261:Glycosylphosphatidylinositols; D007371:Interferon-gamma