T Cell Regulation of Polyclonal B Cell Responsiveness: II. Evidence for a Deficit in T Cell Function in Mice with an X-Linked B Lymphocyte Defect¹

In addition to the x-linked B cell maturation deficit previously reported in CBA/N mice, a functional T cell defect has now been observed. T lymphocyte regulation of the polyclonal PFC response was studied within the context of this x-linked immunodeficiency model. The ability of 1) B cells from (CBA/N × CBA/CaJ)F₁, male mice to respond to nonspecific T cell helper signals and 2) T cells from NCF₁ male mice to provide such signals was investigated under in vitro conditions by using bacterial lipopolysaccharide (LPS) as the polyclonal activator. B lymphocytes from both male and female NCF₁ mice were receptive to T cell help rendered by NCF₁ female T cells. Male T cells, however, were unable to augment polyclonal B cell responses of either NCF₁ male or female B cells to LPS. Treatment with ATS + C reduced the polyclonal response of female but not male spleen cells to LPS. This deficit could not be overcome by the use of greater numbers of NCF₁ male T cells. The observation that this deficiency in T cell regulation is not due to active suppression suggests that the results may be attributable to an intrinsic T cell defect.