Abstract
Ten infants with transient hypogammaglobulinemia were studied to define the cellular basis of their IgG deficiency. The number of circulating B cells were assessed by direct immunofluorescence and was normal in all 10 children. The capacity of mononuclear cells to secrete IgG and IgM following in vitro stimulation with pokeweed mitogen (PWM) was assessed using a reverse hemolytic plaque forming cell (PFC) assay. Cells from all 10 children were deficient in their capacity to generate IgG PFC (1004 ± 543/106 cells vs. 6542 ± 5614/106 cells for normal controls; p<0.0]) but not IgM PFC. T cells and their subsets were enumerated using monoclonal antibodies to T cells (T8), helper/inducer T cells (T4), and suppressor/cytotoxic T cells (T8). All ten patients were found to be selectively deficient in T4+ cells (19.6 ± 5.1% vs. 37 ± 4% for normal controls; p <.01) but not in T3+ cells or T8+ cells. The capacity of the patients' mononuclear cells to release T cell helper factor (a polyclonal B cell activator) following stimulation with PWM and tetanus toxoid antigen was markedly decreased compared to normal controls. Coculture of patients' and parental lymphocytes did not result in suppression of IgG synthesis (mean observed value 134 ± 59% of expected value).
These results suggest that a deficiency of helper T cells underlies the IgG deficiency in transient hypogammaglobulinemia of infancy.
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Geha, R., Mudawwar, F., Rosen, F. et al. 915 DEFICIENCY OF HELPER T CELLS IN TRANSIENT HYPOGAMMA-GLOBULINEMIA. Pediatr Res 15 (Suppl 4), 595 (1981). https://doi.org/10.1203/00006450-198104001-00940
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DOI: https://doi.org/10.1203/00006450-198104001-00940