Sjögren’s syndrome and the epithelial target: A comprehensive review
Author
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Barrera, M. J.
Author
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Bahamondes Cornejo, Valeria Cristina
es_CL
Author
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Sepúlveda, D.
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Author
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Quest, Andrew F. G.
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Author
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Castro, I.
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Author
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Cortés, J.
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Author
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Aguilera, S.
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Author
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Urzúa Tobar, Ulises
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Author
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Molina, C.
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Author
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Pérez, P.
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Author
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Ewert, P.
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Author
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Alliende, C.
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Author
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Hermoso Ramello, Marcela
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Author
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González, S.
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Author
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Leyton Blanca, Cristina
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Author
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González, M. J.
Admission date
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2014-03-14T18:38:29Z
Available date
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2014-03-14T18:38:29Z
Publication date
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2013
Cita de ítem
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Journal of Autoimmunity 42 (2013) 7e18
en_US
Identifier
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doi 10.1016/j.jaut.2013.02.001
Identifier
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https://repositorio.uchile.cl/handle/2250/129315
General note
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Artículo de publicación ISI
en_US
Abstract
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The most difficult component in our understanding of human autoimmunity remains a rigorous
dissection of etiological events. Indeed, the vast literature on autoimmune diseases focuses on the inflammatory
response, with the hope of developing drugs that reduce inflammation. However, there is
increasing recognition that understanding the immunobiology of target tissues will also have direct
relevance to disease natural history, including breach of tolerance. Sjögren’s syndrome is essentially an
epitheliitis and there are major changes to normal architectural salivary organization. We propose that
loss of homeostasis is the initial event that precipitates inflammation and that such inflammatory
response includes not only the adaptive response, but also an intense innate immune/bystander
response. To understand these events this review focuses on the architecture, phenotype, function and
epithelial cell organization. We further submit that there are several critical issues that must be defined
to fully understand epithelial cell immunobiology in Sjögren’s syndrome, including defining epithelial
cell polarity, cellecell and cell to extracellular matrix interactions and a variety of chemical and mechanical
signals. We also argue that disruption of tight junctions induces disorganization of the apical
pole of salivary acinar cells in Sjögren’s syndrome. In addition, there will be a critical role of inflammatory
cytokines in the apico-basal relocation of tight junction proteins. Further, the altered disorganization
and relocation of proteins that participate in secretory granule formation are also dysregulated
in Sjögren’s syndrome and will contribute to abnormalities of mucins within the extracellular matrix.
Our ability to understand Sjögren’s syndrome and develop viable therapeutic options will depend on
defining these events of epithelial cell biology.