Defective specific antiinfluenza virus antibody production in vitro by lymphocytes from patients with ataxia-telangiectasia.

The ability of lymphocytes from 11 patients with ataxia-telangiectasia to produce specific antiinfluenza virus antibody in vitro was evaluated. Lymphocytes from these patients produced markedly less antibody than lymphocytes from normal controls when stimulated with type A influenza viruses. Additional studies were undertaken to evaluate the function of the B cells, T cells, and adherent cells of these patients in specific antibody production. B cells from the AT patients produced one-third to one-half as much antiinfluenza virus antibody as did B cells from normals when stimulated with the polyclonal activator Epstein-Barr virus or, in the two cases studied, when stimulated with influenza virus in the presence of normal HLA-identical T-cells, suggesting that a partial B-cell defect contributed to the deficient antibody response in these patients. Helper T-cell function of T-cells from two patients was evaluated in coculture with their HLA-identical sibling's B cells; these studies revealed that the patients' T-cells could provide less help than normals' T-cells but that this help was not entirely deficient. Furthermore, T-cells from AT patients could provide allostimulated helper T-cell function in coculture with allogeneic normal B cells. Taken together, these results suggest that partial defects of B- and T-cell function both contribute to the decreased antiinfluenza virus antibody production by patients with AT.