Pathogenetic Factors in Sjögren's Syndrome: Recent Developments

Abstract

The study of pathogenetic factors in Sjogren's syndrome ISSI has been problematic, given the overall paucity of coherent data that integrate basic research with clinical findings. The presumed autoimmune nature of SS suggests T-cells, autoantibodies, and cytokines as possible immune factors in the initiation and progression of SS. Recent work on programmed cell death (apoptosis) in SS and its models suggests this as a fourth potential mechanism of disease. These four areas of SS research are reviewed with an emphasis on the most recent findings related to mechanisms of disease. New findings confirm the potential for antigen presentation to T-cells in the salivary glands, as well as involvement of other adhesion molecules with respect to T-cell functions. Restrictions on the receptor repertoires of infiltrating T-cells are discussed, as are new findings on antigenic specificities of these cells. New findings on the specificities of autoantibodies observed in SS are reviewed with an eye toward potential mechanisms for depression of exocrine secretory capacity. Stimulating new findings concerning cytokine production in salivary and lacrimal gland are noted.Particular points of interest with regard to apoptosis include the wide range of values obtained for apoptotic activity in SS and its models, and potential means of resolving discongruent results and the study of factors influencing apoptosis are discussed.

Clinical Profile and Significance of Mucocutaneous Lesions of Primary Sjögren's Syndrome

“…They might play a central role in the initiation and progression of pSS. [ 24 25 ] Cell adhesion molecules are expressed in tunica intima as well as perivascular inflammatory cells, where they involve in the pathogenesis of cutaneous vasculitis. [ 26 ] They might also contribute to pulmonary inflammation and fibrosis,[ 27 ] as well as anemia of chronic diseases by inhibiting proliferation of erythrocyte progenitors, modulating iron metabolism, and suppressing EPO production.…”

Transepithelial bioelectrical properties of rabbit acinar cell monolayers on polyester membrane scaffolds

“…Some severe forms of this condition are associated with autoimmunity in the lacrimal gland, which is characterized by lymphocytic infiltrates containing a large number of CD4 ϩ T cells and immunoglobulin G (IgG) ϩ B cells and smaller numbers of IgM ϩ B cells, macrophages, and dendritic cells (1,35,51,57). These infiltrates produce proinflammatory cytokines, including interleukins-1, -6, -12, and -18, interferon-␥, and tumor necrosis factor-␣ (13,26,32,49,52). It generally is thought that these immune mediators are responsible for parenchymal atrophy and dysfunction of the surviving tissue (17,53,60).…”

Psychiatric disorder as clinical presentation of primary Sjögren's syndrome: two case reports

“…Psychiatric presentation of primary SS also suggests that mental disorders do not occur only as a response to a psychological distress or a reaction to a chronic rheumatological disease, but may be an early manifestation of the same autoimmune process, which presumes the direct immunological activity of SS on the central nervous system (by T cells, autoantibodies, cytokines, or the programmed cell death (apoptosis)) [10]. …”