Cytokine regulation of pulmonary fibrosis in scleroderma

Sergei P. Atamas, Barbara White

Research output: Contribution to journalArticlepeer-review

Abstract

Pulmonary fibrosis occurs in up to 70% of sclerodenna patients and progresses to cause severe restrictive lung disease in about 15% of patients. The mechanisms that cause pulmonary fibrosis in scleroderma remain incompletely understood. Increased amounts of mRNA or protein for multiple profibrotic cytokines and chemokines have been identified in lung tissue or broncholveolar lavage samples from scleroderma patients, when compared to healthy controls. These cytokines include transforming growth factor (TGF)-β, connective tissue growth factor (CTGF), platelet-derived growth factor (PDGF), oncostatin M (OSM), monocyte chemotactic factor-1 and pulmonary and activation-regulated chemokine (PARC). Potential cellular sources of these profibrotic cytokines and chemokines in scleroderma lung disease include alternatively activated macrophages, activated CD8+ T cells, eosinophils, mast cells, epithelial cells and fibroblasts themselves. This review summarizes the literature on involvement of cytokines and chemokines in the development of pulmonary fibrosis in scleroderma.

Original languageEnglish (US)
Pages (from-to)537-550
Number of pages14
JournalCytokine and Growth Factor Reviews
Volume14
Issue number6
DOIs
StatePublished - Dec 2003
Externally publishedYes

Keywords

  • Chemokines
  • Cytokines
  • Fibrosis
  • Lung
  • Scleroderma

ASJC Scopus subject areas

  • Immunology
  • Endocrinology, Diabetes and Metabolism
  • Immunology and Allergy
  • Biochemistry, Genetics and Molecular Biology(all)

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