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. (N Engl J Med. 1981; 305:1307–13.) THE level of serum IgG in the full-term infant is equal to that in the mother or higher, reflecting active transport across the placenta. The level of transplacentally acquired IgG falls rapidly within the first three to four months of postnatal life. Immunoglobulin synthesis begins right after birth, in response to colonization of the gastrointestinal tract, infections, and other antigenic stimulation, and this synthesis is well established after six months of life. This combination of events results in a physiologic hypogammaglobulinemia that is present from four to six months of age.^{1 2 3 4 5} In transient hypogammaglobulinemia of infancy, a delay in immunoglobulin.