Role of cytokines in T cell immunity to a pulmonary Cryptococcus neoformans infection

Biol Signals. Jul-Aug 1996;5(4):215-22. doi: 10.1159/000109193.


The objective of these studies was to present an overview of our studies of the cytokine network and cellular interactions responsible for the T-cell-mediated inflammatory response in the lungs following infection by Cryptococcus neoformans. In a resistant strain of mice, moderately virulent cryptococci were progressively cleared from the lungs after week 1. Characterization of mitogen-induced cytokine production demonstrated that the T cells in the lungs during the first 3 weeks of infection resembled Th0 rather than Th1 cells. In addition, the production of IL-10 (by mitogen-stimulated leukocytes) could promote an increase in the ratio of Th2:Th1 cytokines in short-term in vitro cultures. In vivo, there were increases in the alveolar levels of tumor necrosis factor-alpha and IL-6 at weeks 1-3 and the chemokines monocyte chemoattractant protein-1 at weeks 1-2 followed by macrophage inflammatory protein-1 alpha and ENA-78 at week 3. Overall, the pulmonary inflammatory response to C. neoformans evolved over 5 weeks from granulocytic to mononuclear, suggesting a maturation to a Th1-type response by week 5.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cryptococcosis / immunology*
  • Cytokines / biosynthesis*
  • Interleukin-10 / pharmacology
  • Interleukin-6 / biosynthesis
  • Mice
  • Mice, Inbred CBA
  • Pneumonia, Bacterial / immunology*
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology*
  • Tumor Necrosis Factor-alpha / biosynthesis


  • Cytokines
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Interleukin-10