Deficiency of T helper cells in transient hypogammaglobulinemia of infancy.
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.
D000293:Adolescent; D000361:Agammaglobulinemia / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D005260:Female; D004854:Herpesvirus 4, Human / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000096:biosynthesis; D007136:Immunoglobulins / Q000096:biosynthesis*; D066298:In Vitro Techniques; D007223:Infant; D007958:Leukocyte Count; D008213:Lymphocyte Activation; D008297:Male; D013601:T-Lymphocytes / Q000276:immunology*
D007074:Immunoglobulin G; D007136:Immunoglobulins