Mac-1(+) myelopoiesis induced by CFA: a clue to the paradoxical effects of IFN-gamma in autoimmune disease models

Trends Immunol. 2001 Jul;22(7):367-71. doi: 10.1016/s1471-4906(01)01937-8.

Abstract

The mechanisms accounting for the protective role of endogenous interferon gamma (IFN-gamma) in certain murine autoimmune disease models, versus a disease-promoting role in others, have remained elusive. The protective effect of IFN-gamma might be unique to models that rely on the use of complete Freund's adjuvant (CFA) and whose pathogenesis is predominantly driven by delayed-type hypersensitivity. In these models, IFN-gamma counteracts disease development by inhibiting CFA-induced proliferation of a pathogenically important Mac-1(+) cell population(s). This calls into question our usual conceptualization of the balance between innate and specific immunity in these models, as well as their clinical relevance, particularly when the role of IFN-gamma or related cytokines is considered.

Publication types

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

MeSH terms

  • Animals
  • Arthritis, Rheumatoid / immunology
  • Autoimmune Diseases / immunology*
  • Disease Models, Animal
  • Freund's Adjuvant / immunology*
  • Humans
  • Immunization
  • Interferon-gamma / immunology*
  • Leukopoiesis / immunology*
  • Nuclear Proteins / immunology*
  • Transcription Factors / immunology*

Substances

  • Nuclear Proteins
  • Transcription Factors
  • Interferon-gamma
  • Freund's Adjuvant