Lymphocytic infiltration has also been reported in the salivary glands of healthy subjects with age. SS, which is more prevalent in women than in men (at a ratio of 9:1), is an autoimmune disorder that is characterized by the chronic dysfunction and destruction of exocrine glands, mainly the salivary and lacrimal glands due to lesions chronically infiltrated by lymphocytes, and the majority of SS patients are postmenopausal women. Dry mouth is also a common symptom among patients with several systemic diseases, such as diabetes and Sjögren’s syndrome (SS).

The prevalence of dry mouth (xerostomia) is significantly higher in women than in men and increases with age due, in part, to salivary gland hypofunction. Collectively, the present results indicate that SA-Ts accumulate in SG, contribute to the pathogenesis of age- and SS-related sialadenitis by up-regulating chemokines in epithelial cells, and have potential as therapeutic targets for the treatment of xerostomia caused by these types of sialadenitis. In a mouse model of Sjögren’s syndrome (SS), SA-Ts also accumulated in SG, presumably via CXCL12-CXCR4 signaling.

CD4 + T cells derived from aged mice exhibited stronger in vitro migratory activity toward CXCL13 than those from young mice. The present results showed that SA-Ts and B cells, which express the CXCL13 receptor CXCR5, accumulated in the SG of aged mice, particularly females. Senescence-associated T cells (SA-Ts), which secrete large amounts of atypical pro-inflammatory cytokines, are involved in the pathogenesis of metabolic disorders and autoimmune diseases. An analysis of isolated epithelial cells from SG revealed that the expression levels of the chemokine CXCL13 were elevated in aged mice. We demonstrated that acquired immune cells rather than innate immune cells infiltrated the salivary glands (SG) of aged mice. Although age- and autoimmune-related sialadenitis cause dry mouth (xerostomia), the roles of immunosenescence and cellular senescence in the pathogenesis of sialadenitis remain unknown.

Immunosenescence is characterized by age-associated changes in immunological functions.

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