T cell regulation of polyclonal B cell responsiveness. I. Helper effects of T cells.
Polyclonal activation of murine splenic B lymphocytes to secrete immunoglobulin was shown to be subject to regulation by splenic T cells. By admixture of separated B and T cell populations it was demonstrated that normal fresh splenic T cells were able to augment polyclonal B cell responsiveness to LPS up to several-fold. Optimal collaboration between these two cell types ensued when they were co-cultured in equal numbers. T cell-mediated enhancement of polyclonal B cell responses was dependent upon the ability of T cells to divide and was manifested upon T cell interaction with B cells soon after culture initiation. Originally expounded as a one-signal phenomenon, polyclonal activation of lymphocytes by LPS is, under the circumstances described, attributable instead to two distinct, nonspecific signals acting in concert. The observation that T cells from LPS-nonresponder (C3H/HeJ) mice were deficient in the capacity to enhance polyclonal B cell responsiveness of B cells derived from responder (C3H/HeN) mice implied a direct action of LPS on the involved T cells as well as an active role for the T cell signal in this immunoregulatory event. The novel observation of a functional T cell defect in LPS responsiveness in the C3H/HeJ mouse is discussed in terms of its other cellular defects.
D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D002469:Cell Separation; D002999:Clone Cells / Q000276:immunology; D004306:Dose-Response Relationship, Immunologic; D006462:Hemolytic Plaque Technique; D006648:Histocompatibility; D008070:Lipopolysaccharides / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000528:radiation effects; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D013601:T-Lymphocytes / Q000276:immunology*; D013997:Time Factors
D008070:Lipopolysaccharides