Abstract

Sjögren's syndrome (SS), a systemic autoimmune disease, is characterized by inflammation of exocrine tissues accompanied by a significant loss of their secretory function. Clinical symptoms develop late and there are no diagnostic tests enabling early diagnosis of SS. Thus, particularly to study these covert stages, researchers turn to studying animal models where mice provide great freedom for genetic manipulation and testing the effect of experimental intervention. The present review summarizes current literature pertaining to both spontaneous and extrinsic-factor induced SS-like diseases in mouse models, discussing advantages and disadvantages related to the use of murine models in SS research.

Highlights

  • Assuming that studying a model organism will provide us with relevant information about the organism of our primary interest, investigation of nonhuman animals represents an important pillar in today’s biomedical research

  • The aim of the present review is to provide the reader with an overview and specific information about murine strains that have been proposed as models of s syndrome (SS)

  • SS is a complex autoimmune exocrinopathy that over time often progresses to a systemic disease

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Summary

Introduction

Assuming that studying a model organism will provide us with relevant information about the organism of our primary interest, investigation of nonhuman animals represents an important pillar in today’s biomedical research. Both CBA [97] and SJL [98] mice transgenic for Il12 exhibit focal inflammation within their exocrine glands, with the latter strain showing an additional array of SS-related manifestations, including hyposalivation and modest increases in autoantibody levels upon aging [98] In this context, it should be noted that SJL mice are generally susceptible to pathogenic autoimmunity and are highly prone to develop B-cell lymphoma [99]. The notion that disruption of certain genes triggers distinct pathological changes, almost exclusively limited to the salivary and lacrimal glands, may encourage further investigation of possible interrelationships between organ and lymphocyte development and the etiology of autoimmune diseases In this context, investigation of a T-cell-targeted conditional Id3 knockout strain revealed the strong dependence of the original C57BL/6-Id3–/– strain’s disease profile on ID3-deficient T cells in particular [126]. The intervention caused significant reductions in the number of inflammatory foci and the degree of tissue destruction in the salivary glands [144]

Conclusions
Findings
16. Shaw DR
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