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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

From the Department of Immunopathology, Scripps Clinic and Research Foundation, La Jolla, California 92037

Abstract

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 x 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.

Footnotes

¹ This is Publication No. 1769 from the Department of Immunopathology, Scripps Clinic and Research Foundation, La Jolla, California. This work was supported in part by United States Public Health Service Grant AI-07007, American Cancer Society Grant IM42-G, and Biomedical Research Support Program Grant (RRO-5514).

² Recipient of National Institutes of Health Grant AI-15284 and a Fellowship from The Arthritis Foundation.