Alveolar macrophages from humans and rodents selectively inhibit T-cell proliferation but permit T-cell activation and cytokine secretion

Immunology. 1995 Jan;84(1):142-7.


Alveolar macrophages (AM) are thought to play a key role in the regulation of immune responses within the lung. While it is well established that AM inhibit T-cell proliferation in vitro, it is unclear whether other aspects of the T-cell activation process are also inhibited. The present study demonstrates that AM from rat, mouse and human differ markedly in the potency with which they inhibit mitogen-induced T-cell proliferation, although in humans the degree of inhibition approaches that observed in the animal systems, if antigen (as opposed to mitogen) is employed as the T-cell activating agent. Rodent and human AM also differ in the mechanisms employed to achieve this inhibition; rodent AM appear to utilize reactive nitrogen intermediates, while this does not appear to be the case for human AM. Despite these differences, T cells stimulated in the presence of AM display a similar phenotype in all species examined, i.e. CD3 down-modulation, up-regulation of interleukin-2 receptor (IL-2R) expression and IL-2 production, but inability to respond to IL-2. Thus, AM appear to allow T-cell activation and expression of T-cell effector function, while selectively inhibiting T-cell proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Amino Acid Oxidoreductases / metabolism
  • Animals
  • CD3 Complex / immunology
  • Cell Division
  • Cells, Cultured
  • Cytokines / metabolism*
  • Humans
  • Interleukin-2 / immunology
  • Lymphocyte Activation*
  • Macrophages, Alveolar / metabolism
  • Macrophages, Alveolar / physiology*
  • Mice
  • Mice, Inbred Strains
  • Nitric Oxide Synthase
  • Rats
  • Rats, Inbred Strains
  • Specific Pathogen-Free Organisms
  • T-Lymphocytes / immunology*


  • CD3 Complex
  • Cytokines
  • Interleukin-2
  • Nitric Oxide Synthase
  • Amino Acid Oxidoreductases