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Central nervous system mechanisms in Sjögren’s syndrome

A theory

The origin of the dry eye in Sjogren’s syndrome has hardly been a subject of discussion as it is assumed that lymphoplasmocytic cell infiltration of the tear gland deteriorates its function to such a degree that it causes dry eye. Several observations, however, may not support the concept that tear gland degeneration is the only causative factor in ocular dryness in Sjogren’s syndrome.

Sjogren’s syndrome is thought to be the consequence of a generalised autoimmune induced exocrinopathy resulting in localised symptoms including dry eyes and mouth, and generalised symptoms including fatigue, myalgia, and arthralgia.1 Rarely available epidemiological data suggest a prevalence varying between 1.5–4%, a phenomenon probably at least partly the result of the various classification criteria used.2–4 Important components in the pathogenesis are the emergence5 and persistence of autoimmune T cells6 and a subsequent failure of apoptosis of these activated cells,7 which might result in a persistent stimulation of B cells. Extensive lymphoplasmocytic infiltration of tear and salivary glands is thought to intervene with its secretory function, resulting in dry eyes and mouth.

Even in idiopathic keratoconjunctivitis sicca, usually not thought to be based on generalised autoimmune disease, a local immune driven inflammatory reaction in the tear gland is also thought to interfere with the functional unit comprising the ocular surface, tear gland, and interconnecting reflex arc.8,9 A critical decrease in androgen level leads to atrophy of the lacrimal glands.10 Resulting apoptotic fragments of the interstitial and acinar cells might act as a source of potential autoantigens that subsequently might be presented either by interstitial antigen presenting cells or acinar cells to CD4 cell antigen receptors and start an immune response.11 Several experimental and clinical observations cast doubt on the notion that tear gland degeneration is the …