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In contrast, pathogenic anti-dsDNA antibodies found in SLE are usually of IgG isotype and show high avidity for dsDNA. [15] One possible mechanism for anti-dsDNA and their role in nephritis is the formation of immune complexes that arise by indirect binding to DNA or nucleosomes that are adhered to the glomerular basement membrane (GBM).
the presence of anti-dsDNA, anti-Sm and anti-cardiolipin autoantibodies correlates with the development of systemic lupus erythematosus in particular. [19] The rate of progression is higher in the first five years following the onset of the disease and tends to decrease over time.
In the 1970s, the anti-Ro/anti-SS-A and anti-La/anti-SS-B antibodies were discovered. The Scl-70 antibody was known to be a specific antibody to scleroderma in 1979, however the antigen (topoisomerase-I) was not characterised until 1986. The Jo-1 antigen and antibody were characterised in 1980. [8] [20]
Each will be present in a certain percentage of people who have a particular autoimmune disorder. For instance, up to 80% of those with SLE will have a positive double strand anti-double stranded DNA (anti-dsDNA) autoantibody test, but only about 25–30% will have a positive RNP. Some individuals who do have an autoimmune disorder will have ...
Mutations in the positively charged residues completely abrogate DNA binding and subsequent interferon production through STING. Upon binding dsDNA, cGAS dimerizes and undergoes conformational changes that open up a catalytic nucleotide binding pocket, allowing GTP and ATP to enter. Here they are stabilized through base stacking, hydrogen bonds ...
Graves' disease is a condition characterized by development of autoantibodies to thyroid-stimulating hormone receptors. The binding of the autoantibodies to the receptors results in unregulated production and release of thyroid hormone , [ 23 ] which can lead to stimulatory effects such as rapid heart rate, weight loss, nervousness, and ...
Liver kidney microsomal type 1 antibody (anti-LKM1) is an autoantibody associated with autoimmune hepatitis (AIH). [1] Specifically, its presence in AIH defines type 2 AIH, [ 2 ] [ 3 ] although it has been proposed that anti-liver cytosol type 1 autoantibody without detectable anti-LKM1 can be seen in type 2 AIH. [ 4 ]
HIN2 domain does not block the DNA binding surface of AIM2, hence, DNA binding affinity of AIM2 remains unaffected. It is believed that binding of p202 to DNA and AIM2 might attain a balance between host defense and pathological DNA-induced inflammation. When both p202 and AIM2 are present in equal amounts, there is a competition for dsDNA binding.