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rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-11-28
pubmed:abstractText
This paper articulates a new working hypothesis that explains many of the pathophysiological conditions described under the common rubric "dry eye" as altered states of mucosal immune regulation. A central principle of mucosal immune physiology is that the parenchymal tissues at the effector sites, i.e., the sites at which secretory antibodies are produced, maintain local signaling milieus that support differentiation of IgA+ plasmablasts and survival of IgA+ plasmacytes. These local signaling milieus also support robust regulatory networks that maintain tolerance to commensual microbes, benign antigens, and parenchymal autoantigens. The regulatory networks are mediated by cycles of interactions between successive generations of dendritic cells, which normally mature with tolerogenic functions, and regulatory T cells, which normally reinforce the system's ability to generate new tolerogenic dendritic cells. The systemic endocrine environment controls expression of the local signaling milieu in the mammary gland and in the prostate and male urethral glands. Emerging evidence indicates that the local signaling milieu in the lacrimal gland also is determined, in part, by the systemic endocrine environment. This working hypothesis suggests explanations for the excess incidence of Sjogren syndrome among women and for the mechanisms of several different immunophysiological states in addition to Sjogren syndrome that, like Sjogren syndrome, are associated with the classical symptoms and signs of dry eye. It also comprises a promising rationale for specific new approaches to therapy.
pubmed:language
eng
pubmed:journal
pubmed:status
PubMed-not-MEDLINE
pubmed:month
Oct
pubmed:issn
1542-0124
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
182-92
pubmed:year
2005
pubmed:articleTitle
Mucosal immunity and self-tolerance in the ocular surface system.
pubmed:affiliation
Department of Physiology & Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA. amirchef@usc.edu
pubmed:publicationType
Journal Article