Researchers report defects in the Ets1 gene is linked to characteristics associated with systemic lupus erythematosus immune abnormalities.
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A key finding in the origins of lupus has been discovered. In those with systemic lupus erythematosus, B cells are abnormally activated. This results in the production of antibodies which react against the patient's own tissue, causing a range of symptoms including rashes, joint pain, and fatigue.
Clotting proteins are elevated in the urine of patients with lupus nephritis. The findings provide a new biomarker for the autoimmune disease.
Rare gene variants BLK and BANK1 are present in a substantial percentage of people with Lupus. The genetic variants suppress 1RF5 and type-1 1Fn in B cells, causing dysfunction in the immune cells.
A study in Nature Immunology reports on the mechanism that helps to prevent autoimmune diseases from developing following infection. Researchers report a population of immune cells develop during late stages of the immune response to influenza infection.
According to researchers, rogue B cells can trigger an override that may be responsible for autoimmune attacks and diseases.
Researchers have identified specific cellular events that appear key to the debilitating autoimmune disease, lupus. The findings suggest that blocking this pathway in lupus-triggering cells could be a potent weapon against the disease.
Skin cells may hold the key to explaining why women are more prone to developing autoimmune diseases, such as lupus than men. Researchers found women have more VGLL3 in their skin cells than men. VGLL3 pushes the immune system into overdrive, resulting in the 'self-attacking' autoimmune response, the mouse study revealed. Findings strongly implicate VGLL3 as a pivotal catalyst in sex-based autoimmunity.
Disruptions in maintaining X chromosome inactivation of T cells may explain why women are more prone to developing SLE than males.