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Animal Models of Sjögren’s Syndrome

  • R. W. Hoffman
  • S. E. Walker
Chapter

Abstract

Sjögren’s syndrome was first recognized by Henrich Sjögren (1933) as the triad of keratoconjunctivitis sicca, xerostomia and rheumatoid arthritis. Based upon unique clinical, immunologic and genetic features, two distinct forms of Sjögren’s syndrome, primary and secondary, have since been recognized (Bloch et al. 1965; Fox et al. 1984; Moutsopoulos et al. 1980). The primary form is keratoconjunctivitis sicca associated with xerostomia, whereas secondary Sjögren’s syndrome is the triad of keratoconjunctivitis sicca, xerostomia and a connective tissue disease (Fox et al. 1984; Kaplinsky et al. 1980; McAdam et al. 1976; Whaley and Alspaugh 1985). Sjögren’s syndrome is of interest because it is a common autoimmune disease with significant morbidity (Moutsopoulos et al. 1980). Although extensive studies have provided a large body of information concerning autoantibody production, immune complexes, immunoregulation and immunogenetics, the etiology of Sjögren’s syndrome is not known. Appropriate animal models could greatly advance our understanding of the pathogenesis and treatment of this disorder.

Keywords

Systemic Lupus Erythematosus Salivary Gland Parotid Gland Lacrimal Gland Nictitate Membrane 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Abbreviations

CFA

Complete Freund’s Adjuvant

NZB

New Zealand Black

NZW

New Zealand White

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© Springer-Verlag Berlin Heidelberg 1987

Authors and Affiliations

  • R. W. Hoffman
  • S. E. Walker

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