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The Journal of Immunology, Vol 156, Issue 1 8-11, Copyright © 1996 by American Association of Immunologists

CUTTING EDGE

Impaired T cell-mediated macrophage activation in CD40 ligand-deficient mice

RD Stout, J Suttles, J Xu, IS Grewal and RA Flavell
Department of Microbiology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City 37614-0579, USA.

The expression of the ligand for CD40 (CD40L) is critical for induction of T cell-dependent Ab responses. To examine how critical the expression of CD40L is for induction of cell-mediated immune responses, the ability of T cells from CD40L knockout mice to activate macrophage effector function was assessed. CD4+ T cells from CD40L-knockout mice were fourfold less effective than +/+ T cells in activating the nitric oxide response in allogeneic macrophages. CD40L-knockout T cells that were fixed with paraformaldehyde after a 6-h activation period, a time point at which CD40L dominates the macrophage-activating capability of the T cell, could activate neither macrophage production of inflammatory cytokines (TNF-alpha) nor generation of reactive nitrogen intermediates. After 24 h of activation, however, both CD40L-knockout and +/+ T cells could induce similar but weak responses from the macrophages. This study demonstrates that animals deficient in CD40L expression display a deficiency in T cell-dependent macrophage-mediated immune responses.


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