Early immune events in scleroderma

Research output: Contribution to journalReview article

35 Citations (Scopus)

Abstract

A number of humoral and cellular immune abnormalities are present in patients with early scleroderma (systemic sclerosis). Most of these abnormalities reflect ongoing autoimmune reactions of the cellular and humoral types, resulting in a variety of autoantibodies to cellular and tissue constituents. Evidence exists for a defect(s) in immunoregulation favoring excessive helper T-cell activity. The presence of circulating cytokines and shed interleukin-2 receptors suggest ongoing cellular immune reactions are occurring, generating cytokines and lymphokines that are capable of effecting the vascular and fibrotic lesions that are hallmarks of the disease. Future directions for research are suggested that would focus on determining if, and at what point, fibroblasts might function autonomously to generate excessive matrix components and on determining the nature of the original antigenic stimulus that starts the scleroderma process.

Original languageEnglish (US)
Pages (from-to)125-139
Number of pages15
JournalRheumatic Disease Clinics of North America
Volume16
Issue number1
StatePublished - 1990

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Cytokines
Lymphokines
Systemic Scleroderma
Interleukin-2 Receptors
Helper-Inducer T-Lymphocytes
Autoantibodies
Blood Vessels
Fibroblasts
Research
Direction compound

All Science Journal Classification (ASJC) codes

  • Rheumatology

Cite this

Early immune events in scleroderma. / Postlethwaite, Arnold.

In: Rheumatic Disease Clinics of North America, Vol. 16, No. 1, 1990, p. 125-139.

Research output: Contribution to journalReview article

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AB - A number of humoral and cellular immune abnormalities are present in patients with early scleroderma (systemic sclerosis). Most of these abnormalities reflect ongoing autoimmune reactions of the cellular and humoral types, resulting in a variety of autoantibodies to cellular and tissue constituents. Evidence exists for a defect(s) in immunoregulation favoring excessive helper T-cell activity. The presence of circulating cytokines and shed interleukin-2 receptors suggest ongoing cellular immune reactions are occurring, generating cytokines and lymphokines that are capable of effecting the vascular and fibrotic lesions that are hallmarks of the disease. Future directions for research are suggested that would focus on determining if, and at what point, fibroblasts might function autonomously to generate excessive matrix components and on determining the nature of the original antigenic stimulus that starts the scleroderma process.

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