Surface Properties of Activated Macrophages: Sensitized Lymphocytes, Specific Antigen and Lymphokines Reduce Expression of Antigen F4/80 and FC and Mannose/Fucosyl Receptors, but Induce Ia

  • R. A. B. Ezekowitz
  • S. Gordon
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 155)


The term macrophage activation was introduced by Mackaness in the 1960’s to describe the enhanced microbicidal activity of macrophages from animals with acquired immunity to infection with facultative intracellular pathogens (1). Attempts have been made since that time to define the properties of macrophage activation in terms of morphological changes, biochemical or membrane events and correlate these with microbicidal and tumoricidal activity (2,3,4). After infection with bacillus Calmette-Guérin (BCG), the host may acquire immunity to specific secondary challenge, protection against unrelated virulent organisms such as Listeria monocytogenes and increased resistance to transplantable tumors (5–7). Macrophages from such animals spread rapidly in cultures, secrete high levels of hydrogen peroxide (8) and plasminogen activator (9) and display enhanced tumoricidal activity (10). We have shown that infection of the mouse peritoneal cavity by BCG markedly alters the surface properties of the macrophages induced, compared with uninfected controls, or after injection of thioglycollate broth (11). Quantitative binding assays with radio-labeled ligands or monoclonal antibodies showed that BCG-activated peritoneal macrophages (BCG-PM) express reduced antigen F4/80, (a macrophage specific antigen of MW 160,000), Fc receptors and mannose specific receptor activity, but have enhanced Ia antigen and increased secretion of hydrogen peroxide and plasminogen activator. We have also shown that (a) these alterations in the plasma membrane make it possible to distinguish between activated and non-activated macrophages, and (b) all changes of macrophage activation by BCG are dependent upon ‘T’ lymphocytes and specific antigen. However, studies with nude mice indicate that the activation phenotype may also arise by an independent pathway. The altered surface properties are stable, occur in a co-ordinate manner, independent of a particular agent and can be induced in vivo and in vitro.


Plasminogen Activator Peritoneal Macrophage Purify Protein Derivative Resident Macrophage Tumoricidal Activity 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Mackaness, G. B., J. Exp. Med. 116:381, 1962.PubMedCrossRefGoogle Scholar
  2. 2.
    North, R. J., J. Immunol. 121:806, 1978.PubMedGoogle Scholar
  3. 3.
    Karnovsky, M. L., and Lazdins, J. K., J. Immunol. 121:809, 1978.PubMedGoogle Scholar
  4. 4.
    Cohn, Z. A., J. Immunol. 121:813, 1978.PubMedGoogle Scholar
  5. 5.
    Blanden, R. N., Lefford, M. J., and Mackaness, G., J. Exp. Med. 129:1079, 1969.PubMedCrossRefGoogle Scholar
  6. 6.
    Nathan, C. F., in “Mononuclear Phagocytes” (R. van Furth, ed.), p. 1165, Martinus, Nijhoff Publishers, 1980.Google Scholar
  7. 7.
    Nelson, D. S., “Immunobiology of the Macrophage”, Academic Press, Inc., London, 1976.Google Scholar
  8. 8.
    Nathan, C. F., and Root, R. K., J. Exp. Med. 146:1648, 1977.PubMedCrossRefGoogle Scholar
  9. 9.
    Gordon, S., and Cohn, Z. A., J. Exp. Med. 147:1175, 1978.PubMedCrossRefGoogle Scholar
  10. 10.
    Old, L. J., Benacerraf, B., Clarke, D. A., Carswell, C. E., and Stockert, E., Cancer Res. 21:1281, 1961.PubMedGoogle Scholar
  11. 11.
    Ezekowitz, R. A. B., Austyn, J., Stahl, P. D., and Gordon, S., J. Exp. Med. 154:60, 1981.PubMedCrossRefGoogle Scholar
  12. 12.
    Stahl, P. D., Schlesinger, P. H., Sigardson, E., Rodman, J. S., and Lee, Y. S., Cell 19:207, 1980.PubMedCrossRefGoogle Scholar
  13. 13.
    Stahl, P., and Gordon, S., J. Cell Biol. 93:49, 1982.PubMedCrossRefGoogle Scholar
  14. 14.
    Unkeless, J. C., J. Exp. Med. 150:580, 1979.PubMedCrossRefGoogle Scholar
  15. 15.
    Nathan, C., and Cohn, Z. A., J. Exp. Med. 152:198, 1980.PubMedCrossRefGoogle Scholar
  16. 16.
    Austyn, J., and Gordon, S., Eur. J. Immunol. 11:805, 1981.PubMedCrossRefGoogle Scholar
  17. 17.
    McMaster, W. R., and Williams, A. F., Immunol. Rev. 47:117, 1979.PubMedCrossRefGoogle Scholar
  18. 18.
    Springer, T., Galfre, G., Secher, D. S., and Milstein, C., Eur. J. Immunol. 4:91, 1979.Google Scholar
  19. 19.
    Cummings, N. P., Pabst, M. J., and Johnston, R. B. Jr., J. Exp. Med. 152:1659, 1980.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1982

Authors and Affiliations

  • R. A. B. Ezekowitz
    • 1
  • S. Gordon
    • 1
  1. 1.Sir William Dunn School of PathologyUniversity of OxfordOxfordUK

Personalised recommendations