Recent advances in understanding molecular mechanisms in the pathogenesis and antibody profile of Sjögren's syndrome

Curr Rheumatol Rep. 2003 Aug;5(4):311-6. doi: 10.1007/s11926-003-0010-z.

Abstract

Sjögren's syndrome is a chronic autoimmune and rheumatic disorder of the mucous membranes caused by a lack of proper exocrine secretions, with prominent sicca complaints. The molecular mechanisms of the pathogenesis are virtually unknown, although progress has been made with regard to chemokines, B cell activating factor, and apoptosis. A large number of autoantibodies have been reported in Sjögren's syndrome, some of which relate to impairment of glandular function. Sjögren's syndrome is a female-dominant disease with a late age of onset; most patients contract the disease at the age of 40 to 50 years. Lately, attention has been drawn to the effects of adrenopause in Sjögren's syndrome and on dehydroepiandrosterone and its intracrine metabolism in target tissues. This can influence the maintenance and remodeling of exocrine glands and may explain, in part, another important disease symptom--fatigue.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Age of Onset
  • Apoptosis / immunology
  • Aquaporins / metabolism
  • Autoantibodies / metabolism
  • Autoimmune Diseases / immunology
  • Autoimmune Diseases / physiopathology*
  • B-Lymphocytes / immunology
  • Female
  • Humans
  • Rheumatic Diseases / immunology
  • Rheumatic Diseases / physiopathology*
  • Sjogren's Syndrome* / drug therapy
  • Sjogren's Syndrome* / immunology
  • Sjogren's Syndrome* / physiopathology
  • Synaptic Transmission / immunology

Substances

  • Aquaporins
  • Autoantibodies