Sjögren’s syndrome (SS) of humans and SS-like (SjS-like) diseases in various mouse models are best classified as systemic, hypersensitive Type II inflammatory-based rheumatic diseases characterized by chronic progressive immune attacks primarily against the salivary and lacrimal glands, resulting, respectively, in dry mouth (stomatitis sicca/xerostomia) and dry eye (keratoconjunctivitis sicca/xerophthalmia) diseases [1–5]. In humans, the vast majority of SS patients are post-menopausal women, implicating a strong hormone influence. In addition to the apparent primary sites of autoimmunity, multiple tissues may become involved including the GI tract, skin, lungs, vasculature, kidneys, bladder and vagina. Furthermore, perhaps 20% of SS patients exhibit various neuropathies, including sensory, peripheral, cranial and myelopathic complications [6]. Cognitive impairments such as dementia, lack of concentration, memory loss and various psychiatric disorders (ranging from depression to anxiety) are also noted in patients during clinic visits [7–9], a condition often referred to as ‘mental fogginess’. Involvement of the musculature can lead to fibromyalgia-like symptoms and chronic fatigue [3, 4], the latter being one of the most prevalent complaints. Many of these secondary complaints are thought to be a consequence of circulating interferons and autoantibodies.
