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Platelet contributions to the pathogenesis of systemic sclerosis

Arnold E Postlethwaite1, Thomas M Chiang

  • 1Division of Connective Tissue Diseases, Department of Medicine and Molecular Sciences, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA. apostlethwai@utmem.edu

Current Opinion in Rheumatology
|October 6, 2007
PubMed

Insights

Platelets play a significant role in systemic sclerosis (SSc) pathogenesis. SSc platelets show increased activation and express collagen receptors, contributing to inflammation and fibrosis in this autoimmune disease.

Area of Science:

  • Immunology
  • Hematology
  • Rheumatology

Background:

  • Systemic sclerosis (SSc) is a complex autoimmune disease characterized by fibrosis.
  • Platelets are increasingly recognized for their role beyond hemostasis, particularly in inflammatory and fibrotic conditions.

Purpose of the Study:

  • To review the general contributions of platelets to systemic sclerosis.
  • To highlight recent advances in characterizing the phenotype of platelets in SSc.

Main Methods:

  • Literature review focusing on platelet function and phenotype in SSc.
  • Analysis of studies detailing platelet activation markers and receptor expression.

Main Results:

  • Evidence supports varying degrees of platelet activation and aggregation in SSc.
  • Systemic sclerosis platelets overexpress a type I collagen receptor (65 kDa), enhancing their binding to collagen.
  • Activated SSc platelets exhibit enhanced phosphatidylinositol-3 kinase signaling, indicative of an activated phenotype, potentially driven by autoimmune factors.

Conclusions:

  • Platelet contributions to SSc pathogenesis are substantial.
  • The role of platelets in SSc may be underestimated in gene profiling studies due to low platelet RNA content.
Abstract

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