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An Alternative Perspective to the Immune Response in Autoimmune Exocrinopathy: Induction of Functional Quiescence Rather Than Destructive Autoaggression
Author(s) -
HUMPHREYSBEHER M. G.,
BRAYER J.,
YAMACHIKA S.,
PECK A. B.,
JONSSON R.
Publication year - 1999
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1999.00490.x
Subject(s) - pathogenesis , immune system , exocrine gland , autoimmunity , mononuclear cell infiltration , inflammation , salivary gland , immunology , pathology , vasoactive intestinal peptide , biology , medicine , receptor , endocrinology , secretion , neuropeptide
Sjögren's syndrome is characterized by dryness of the eyes and the mouth due to mononuclear cell infiltration of the lacrimal and salivary glands. The aetiology is unknown but autoimmunity is considered to play a significant role in the pathogenesis. Recent studies have focused on the fact that tear and salivary flow involves an entire functional system that includes the mucosal surfaces with adnexes (the site of inflammation), efferent nerve signals sent to the midbrain (lacrimal and salivary response region), and afferent neural signals from the brain to the acinar/ductal epithelial structures in the gland. Mononuclear cell infiltration in exocrine glands can lead to glandular destruction, suggested to be mediated through apoptosis. However, the functional impairment of exocrine glands could be regulated by cytokines and/or antibodies against the muscarinic M3 receptor by inhibiting the neural stimulation of the residual glands. This review discusses the possibility that the pathogenesis of Sjögren's syndrome comprises aberrant immune‐mediated neuro‐hormonal events.