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In Sjogren’s syndrome, the body’s immune cells go rogue and start attacking various exocrine glands, which are glands that pour their secretions into a duct; most commonly the salivary glands and the lacrimal, or tear, glands.
Pieces of the pathogen called antigens are then presented on a major histocompatibility complex class II molecule, or MHC-class II molecule - which is like a serving platter for antigens. An antigen presenting cell then searches for a T cell that can bind to the antigen.
Once found, binding to the antigen helps activate this T cell, which then releases proinflammatory cytokines, or signaling molecules, that recruit more immune cells - ultimately leading to inflammation.
The exact cause for Sjogren's syndrome is unknown, but it seems to be related to both genetic and environmental factors.
Genetic factors include genes which code for specific types of MHC class II molecules, called human leukocyte antigen, or HLA genes. Specifically HLA- DRW52, HLA- DQA1, or HLA- DQB1.
Environmental factors include an infection of exocrine glands like the salivary and lacrimal glands. Infections can damage the cells of the salivary gland, and expose their cell components, including their DNA, RNA, and histones to circulating immune cells.
Sjogren's syndrome is an autoimmune disease in which the body's immune cells attack various moisture-producing exocrine glands, which normally pour their secretions into various ducts in the body, such as the salivary and the lacrimal glands. This results in the development of a dry mouth and dry eyes. Other symptoms can include dry skin, a chronic cough, vaginal dryness, numbness in the arms and legs, feeling tired, and muscle and joint pains. Treatment of Sjogren's syndrome typically involves medications to suppress the immune response, like corticosteroids; and also medications that increase the exocrine secretions like pilocarpine.
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