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Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Deficiency of T helper cells in transient hypogammaglobulinemia of infancy.
New England Journal of Medicine 1981 November 27
We studied 17 patients with transient hypogammaglobulinemia of infancy to define the immunologic defect responsible for this disorder. The number of circulating B cells in these patients was normal, as was the ability of the B cells to synthesize immunoglobulins when stimulated with Epstein-Barr virus, a direct B-cell activator. However, the capacity of the B cells to synthesize IgG in response to pokeweed mitogen, a T-cell-dependent B-cell activator, was depressed. Experiments with cultured lymphocytes indicated that excess suppressor-cell activity was not present in these patients, but that their T cells were deficient in providing help to B cells from their normal parents. A numerical deficiency in T4-positive (T4+) helper cells was found. Patients who had recovered from the disorder had a normal number of T4+ helper cells. Our results indicate that a numerical, as well as a functional, deficiency in helper T cells underlies the deficiency in IgG production in transient hypogammaglobulinemia of infancy.
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