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Previous Volume 305:1307-1313 November 26, 1981 Number 22 Next

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Abstract

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.

This article has been cited by other articles:

• Goldman, A. S., Miles, S. E., Rudloff, H. E., Palkowetz, K. H., Schmalstieg, F. C. Jr. (1999). Immunodeficiency Due to a Unique Protracted Developmental Delay in the B-Cell Lineage. CVI 6: 161-167 [Abstract] [Full Text]