Abstract
Sjogren’s syndrome is a systemic autoimmune condition centred around salivary gland dysfunction and atrophy. There are a plethora of antibodies that mark the decline of the salivary glands, most of which relate to apoptopic mediated destruction of acinar cells. The best known of these autoantibodies, anti-Ro and anti-La form part of the diagnostic criteria for the condition. An emerging viewpoint in recent years is that glandular dysfunction precedes rather than follows glandular atrophy and attention has shifted to the interface between the immune system and the secretory process. An autoantibody against the muscarinic type 3 acetylcholine receptor occupies precisely this position because it inhibits the acetylcholine receptor which controls salivary and lacrimal fluid secretion. The consequence of identifying an autoantibody that can cause rather than simply reflect the disease process are manifold and could have a huge impact on development of therapeutic treatments. Furthermore, a “functional” autoantibody directed against an important component of the autonomic nervous system could also account for some of the extraglandular features of Sjogren’s syndrome.
Keywords: Autoantibody, lacrimal, muscarinic type 3 receptor, salivary, sjogren’s syndrome, xeropthalmia, xerostomia, systemic autoimmune, salivary gland dysfunction, plethora, atrophy, immune system, secretory process, lacrimal fluid secretion, autonomic nervous system.
Current Pharmaceutical Biotechnology
Title:Autoantibodies and Sjogren’s Syndrome: A Physiologist’s Perspective
Volume: 13 Issue: 10
Author(s): Peter M. Smith and Luke J. Dawson
Affiliation:
Keywords: Autoantibody, lacrimal, muscarinic type 3 receptor, salivary, sjogren’s syndrome, xeropthalmia, xerostomia, systemic autoimmune, salivary gland dysfunction, plethora, atrophy, immune system, secretory process, lacrimal fluid secretion, autonomic nervous system.
Abstract: Sjogren’s syndrome is a systemic autoimmune condition centred around salivary gland dysfunction and atrophy. There are a plethora of antibodies that mark the decline of the salivary glands, most of which relate to apoptopic mediated destruction of acinar cells. The best known of these autoantibodies, anti-Ro and anti-La form part of the diagnostic criteria for the condition. An emerging viewpoint in recent years is that glandular dysfunction precedes rather than follows glandular atrophy and attention has shifted to the interface between the immune system and the secretory process. An autoantibody against the muscarinic type 3 acetylcholine receptor occupies precisely this position because it inhibits the acetylcholine receptor which controls salivary and lacrimal fluid secretion. The consequence of identifying an autoantibody that can cause rather than simply reflect the disease process are manifold and could have a huge impact on development of therapeutic treatments. Furthermore, a “functional” autoantibody directed against an important component of the autonomic nervous system could also account for some of the extraglandular features of Sjogren’s syndrome.
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Cite this article as:
M. Smith Peter and J. Dawson Luke, Autoantibodies and Sjogren’s Syndrome: A Physiologist’s Perspective, Current Pharmaceutical Biotechnology 2012; 13 (10) . https://dx.doi.org/10.2174/138920112802273218
DOI https://dx.doi.org/10.2174/138920112802273218 |
Print ISSN 1389-2010 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4316 |
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