Macrophage activation and innate resistance to infection in SCID mice

Immunobiology. 1994 Oct;191(4-5):424-31. doi: 10.1016/S0171-2985(11)80448-1.


Resistance to infection against a variety of pathogens requires the co-ordinated interaction of both the innate and acquired immune responses. Mice bearing the SCID mutation are devoid of T and B cells but retain elements of the innate immune system including natural killer (NK) cells, macrophages, granulocytes and complement proteins. Using the SCID model we have identified a T cell independent mechanism of macrophage activation mediated by the secretion of IFN-gamma from NK cells. This process occurs in response to a variety of parasites and bacteria including Listeria monocytogenes, and is strictly regulated both in vitro and in vivo by cytokines such as IL-2 and IL-10. Here we discuss the mechanisms of NK cell activation and regulation and describe a new model of opportunistic infection in SCID mice with the AIDS related pathogen Cryptosporidium parvum.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Immunity, Innate*
  • Interferon-gamma / biosynthesis
  • Killer Cells, Natural / immunology
  • Listeriosis / etiology
  • Listeriosis / immunology
  • Macrophage Activation / immunology*
  • Mice
  • Mice, SCID / immunology*
  • T-Lymphocytes / immunology


  • Interferon-gamma