Abstract
Coronaviruses are a large family of viruses that can cause mild infections, such as the common cold, to more severe clinical manifestations. On 31 December 2019, cases of pneumonia of unknown etiology were reported in Wuhan, China. On 7 January 2020, the name of the disease was named Coronavirus Disease-2019 (COVID-19), and the agent was named SARS-CoV-2. Studies have shown that the worsening of the disease was immunopathological. Clinical progression rapidly worsens as a result of the onset of a severe immunological response to the virus and the elevation of cytokine levels. In addition to the intensified immunological response, some studies have focused on the effect of autoantibodies on the disease. Autoantibodies targeting their own cells and tissues have been reported in some patients. Although it is not known exactly how these autoantibodies are formed, theories are focused on the sensitization of the immune system to one's own cells and that some of the epitopes of the virus may resemble our antigens. Autoantibodies have been shown to increase the severity of the disease and prolong the healing process. (Anti-nücleer antibody) ANA, anti-phospholipid antibodies and anti-type 1 interferon antibodies were detected most frequently in COVID-19 cases. Rarely, other types of autoantibodies -Anti-neutrophil cytoplasmic antibody (ANCA), Anti-cyclic citrulline peptide antibody (Anti-CCP) etc.- have been encountered. More comprehensive prospective scientific studies should be conducted on the formation of autoantibodies in COVID-19 disease.
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