Fibrotic disease and the T(H)1/T(H)2 paradigm

Nat Rev Immunol. 2004 Aug;4(8):583-94. doi: 10.1038/nri1412.


Tissue fibrosis (scarring) is a leading cause of morbidity and mortality. Current treatments for fibrotic disorders, such as idiopathic pulmonary fibrosis, hepatic fibrosis and systemic sclerosis, target the inflammatory cascade, but they have been widely unsuccessful, largely because the mechanisms that are involved in fibrogenesis are now known to be distinct from those involved in inflammation. Several experimental models have recently been developed to dissect the molecular mechanisms of wound healing and fibrosis. It is hoped that by better understanding the immunological mechanisms that initiate, sustain and suppress the fibrotic process, we will achieve the elusive goal of targeted and effective therapeutics for fibroproliferative diseases.

Publication types

  • Review

MeSH terms

  • Animals
  • Chemokines / metabolism
  • Fibroblasts / metabolism
  • Fibrosis / immunology*
  • Fibrosis / metabolism
  • Fibrosis / therapy
  • Humans
  • Interleukin-13 / metabolism
  • Macrophages / metabolism
  • Th1 Cells / immunology*
  • Th1 Cells / metabolism
  • Th2 Cells / immunology*
  • Th2 Cells / metabolism
  • Transforming Growth Factor beta / metabolism


  • Chemokines
  • Interleukin-13
  • Transforming Growth Factor beta