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TNF pathophysiology in murine models of chronic inflammation and autoimmunity

George Kollias1

  • 1Biomedical Sciences Research Center Al Fleming, Vari, Greece. g.kollias@fleming.gr

Seminars in Arthritis and Rheumatism
|April 27, 2005
PubMed

Insights

Tumor necrosis factor (TNF) plays a dual role in disease, mediating both beneficial and harmful responses. Selective inhibition of TNF receptors shows promise for treating chronic inflammatory diseases.

Area of Science:

  • Immunology and Molecular Biology
  • Inflammation and Autoimmune Diseases

Background:

  • Tumor necrosis factor (TNF) and its receptors are crucial in disease pathogenesis.
  • TNF mediates both beneficial and detrimental responses through complex molecular and cellular pathways.
  • Posttranscriptional regulation, secretion, and postreceptor actions of TNF contribute to disease.

Purpose of the Study:

  • To elucidate the specific functions of TNF and its receptors in disease.
  • To understand the molecular and cellular mechanisms underlying TNF's effects.
  • To explore the potential of selective TNF receptor inhibition in treating chronic inflammatory diseases.

Main Methods:

  • Utilizing experimental animal models to study TNF function.
  • Analyzing molecular and cellular pathways involved in TNF signaling.
  • Investigating TNF receptor heterogeneity in disease models.

Main Results:

  • TNF exhibits diverse roles, contributing to both disease suppression and inflammatory damage.
  • Evidence suggests distinct TNF receptor usage in different disease contexts.
  • Heterogeneity in TNF receptor function is observed in murine models.

Conclusions:

  • Selective TNF receptor inhibition may offer advantages over broad anti-TNF therapies.
  • Targeting specific TNF receptor pathways could be a more effective strategy for chronic inflammatory diseases.
  • Further research into TNF receptor heterogeneity is warranted for therapeutic development.

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