Journal
CRITICAL REVIEWS IN ORAL BIOLOGY & MEDICINE
Volume 15, Issue 3, Pages 156-164Publisher
INT AMER ASSOC DENTAL RESEARCHI A D R/A A D R
DOI: 10.1177/154411130401500304
Keywords
apoptosis; autoimmunity; protease; autoantigen; autoantibody; structure; caspase; granzyme B
Categories
Funding
- NIAMS NIH HHS [AR44684] Funding Source: Medline
- NIDCR NIH HHS [R37 DE12354] Funding Source: Medline
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The etiology and pathogenic mechanisms underlying Sjogren's syndrome (SS) remain unclear. Recent studies have emphasized that the specific autoantibodies that occur in a high proportion of patients with SS may provide important insights into the circumstances that initiate and propagate tissue damage in this disease. Although autoantigens targeted in systemic autoimmune diseases share little in common in terms of structure, subcellular distribution, or function in normal cells, these molecules are unified by becoming clustered and concentrated in the surface blebs of apoptotic cells. Furthermore, their structure is altered during some types of cell death to generate structures not previously generated during development and homeostasis. This review highlights the susceptibility of SS autoantigens to undergoing such structural changes during activation of immune effector pathways, and synthesizes a model of SS incorporating these concepts. An understanding of the mechanisms responsible for activating the specific immune response in SS, and the role of specific immune effector pathways in propagating both the autoimmune response and tissue damage, is of potential therapeutic importance.
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