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CD40 ligand trimer enhances the response of CD8+ T cells to Mycobacterium tuberculosis

Buka Samten1, Benjamin Wizel, Homayoun Shams

  • 1Department of Microbiology and Immunology and Center for Pulmonary and Infectious Disease Control, University of Texas Health Center, Tyler, TX 75708, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|March 11, 2003
PubMed

Insights

Recombinant CD40 ligand trimer (CD40LT) boosts CD8(+) T cell responses against tuberculosis. This immune enhancement involves increased interferon-gamma (IFN-γ) production and improved killing of infected cells.

Area of Science:

  • Immunology
  • Cellular Biology
  • Infectious Diseases

Background:

  • Tuberculosis (TB) remains a significant global health challenge.
  • CD8(+) T cells play a crucial role in controlling Mycobacterium tuberculosis (M.tb) infection.
  • Enhancing CD8(+) T cell effector functions is a potential therapeutic strategy for TB.

Purpose of the Study:

  • To investigate the impact of recombinant CD40 ligand trimer (CD40LT) on the functional capacity of CD8(+) T cells from healthy tuberculin reactors when co-cultured with M.tb-infected monocytes.
  • To elucidate the mechanisms underlying CD40LT-mediated enhancement of CD8(+) T cell responses.

Main Methods:

  • Peripheral blood CD8(+) T cells from tuberculin-positive donors were cultured with M.tb-infected autologous monocytes.
  • Recombinant CD40LT was added to assess its effect on T cell function.
  • Interferon-gamma (IFN-γ) production, transcription factor expression (phosphorylated CREB, c-Jun), cytotoxic T lymphocyte (CTL) activity, and expression of cytotoxic molecules (perforin, granulysin, Fas ligand) were measured.

Main Results:

  • CD40LT significantly enhanced the production of IFN-γ by M.tb-responsive CD8(+) T cells, increasing both the number of producing cells and the amount of IFN-γ per cell.
  • CD40LT-induced IFN-γ production was dependent on IL-12 and IL-18, but not IL-15.
  • CD40LT upregulated phosphorylated CREB and c-Jun, transcription factors known to promote IFN-γ transcription.
  • CD40LT augmented the capacity of CD8(+) T cells to lyse M.tb-infected monocytes, correlating with increased perforin and granulysin expression.

Conclusions:

  • CD40LT effectively enhances the effector functions of CD8(+) T cells against Mycobacterium tuberculosis.
  • The mechanism involves increased IFN-γ production, transcription factor activation, and enhanced cytotoxic potential.
  • CD40LT represents a promising immunomodulatory agent for boosting cellular immunity in tuberculosis.

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