Macrophage inflammatory proteins MIP-1 and MIP-2 are involved in T cell-mediated neutrophil recruitment

J Leukoc Biol. 1992 Sep;52(3):303-6. doi: 10.1002/jlb.52.3.303.


Mice intraperitoneally (i.p.) infected with Mycobacterium bovis bacille Calmette-Guérin (BCG) respond to an i.p. challenge with mycobacterial antigen with an acute and extensive accumulation of neutrophils. This influx was not mimicked by the inoculation of recombinant interferon-gamma (IFN-gamma) or tumor necrosis factor alpha (TNF-alpha). The antigen-induced recruitment of neutrophils was not affected by coinoculation of anti-IFN-gamma antibodies, was enhanced by anti-TNF-alpha antisera, and was significantly reduced by antisera against macrophage inflammatory proteins MIP-1 and MIP-2. The latter two sera had no additive effects. We hypothesize that mycobacteria-specific T cells are triggered by antigen to secrete MIP-1 and MIP-2, which directly mediate, at least partly, the influx of neutrophils that takes place in this model.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chemokine CCL4
  • Chemokine CXCL2
  • Cytokines / immunology*
  • Female
  • Interferon-gamma / immunology*
  • Macrophage Inflammatory Proteins
  • Mice
  • Mice, Inbred C57BL
  • Monokines / immunology*
  • Mycobacterium avium / immunology*
  • Mycobacterium bovis / immunology*
  • Neutrophils / immunology*
  • Neutrophils / physiology
  • T-Lymphocytes / immunology*
  • Tumor Necrosis Factor-alpha / immunology*


  • Chemokine CCL4
  • Chemokine CXCL2
  • Cytokines
  • Macrophage Inflammatory Proteins
  • Monokines
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma