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,
Departments of
*
Microbiology and Immunology and
Medicine and
Center for Pulmonary and Infectious Disease Control, University of Texas Health Center, Tyler, TX 75708;
Department of Internal Medicine, University of North Texas Health Sciences Center, Fort Worth, TX 76107;
¶ Amgen, Seattle, WA 98101; and
|| Division of Immunology and Transplantation Biology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305
We investigated the effect of recombinant CD40 ligand trimer (CD40LT) on the functional capacity of peripheral blood CD8+ T cells from healthy tuberculin reactors that were cultured with Mycobacterium tuberculosis-infected autologous monocytes. CD40LT enhanced the capacity of M. tuberculosis-responsive CD8+ T cells to produce IFN-
by increasing the number of IFN--producing CD8+ T cells and the amount of IFN- produced per cell. CD40LT-induced IFN- production was dependent on production of IL-12 and IL-18, but did not require IL-15. CD40LT up-regulated expression of the transcription factors phosphorylated CREB and c-Jun, both of which have been previously shown to stimulate IFN- mRNA transcription by binding to the IFN- promoter. CD40LT also enhanced the capacity of CD8+ T cells to lyse M. tuberculosis-infected monocytes, and increased CTL activity was associated with higher expression of perforin and granulysin, but not of Fas ligand. We conclude that CD40LT can enhance CD8+ T cell effector function in response to M. tuberculosis.
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