Systemic lupus erythematosus (SLE), also called lupus, is an autoimmune disorder characterized by the immune system attacking the body's own tissues and organs, leading to inflammation and damage. The severity of the disease varies, from mild cases only involving the skin to severe cases affecting multiple organs, including the brain. Lupus sufferers experience flares, or intervals of active disease, and remissions in disease. The disease most predominantly occurs in women of childbearing age, but also affects children, adolescents, and men. While the cause of lupus is still unknown, various genetic, environmental, and infectious causes have been associated with its development. Current treatments for lupus vary depending on the extent of the disease, and may change over time. Some medications used to ease symptoms include nonsteroidal anti-inflammatory drugs, antimalarial drugs, corticosteroids, and immunosuppressive medications, though many of these drugs carry their own risks.
How cells recognize pathogens and alert the immune system swiftly is a fundamental process of high importance for the survival of any species, including humans.
Working alongside colleagues in Mainz, Bern, Hannover and Bonn, researchers from Charité - Universitätsmedizin Berlin, the Berlin Institute of Health and the German Rheumatism Research Center Berlin were able to show how the microbiome helps to render the immune system capable of responding to pathogens.
Chandra Mohan, a Hugh Roy and Lillie Cranz Cullen Endowed Professor of biomedical engineering at the University of Houston, and his colleagues have identified a race-specific variance in the urinary biomarker proteins of lupus nephritis (LN) in patients.
Macrophages are immune cells that patrol the body looking for potential threats like viruses, bacteria, and cancer cells, and engulf and destroy them.
Scientists have discovered that patients suffering from OCD have increased levels of a protein called Immuno-moodulin (Imood) in their lymphocytes.
According to a new study performed by the University of Wisconsin-Madison, deleting a gene from insulin-producing cells prevents the development of Type 1 diabetes in mice, by sparing the cells from being attacked by their own immune system.
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