There are many factors associated with the development of autoimmune diseases. It is known that viral infections can be the triggers of these diseases [
1,
2]. Since the end of 2019, the world has been faced with the global COVID19 pandemic caused by coronavirus 2 (SARS-CoV-2). As knowledge about the virus and its broad pathogenetic potential increased, evidence emerged of the development of various autoantibodies and autoimmune diseases following COVID19 infections [
3‐
5]. COVID-19 was associated with a polyclonal autoreactive B cell activation reflected by an increased number of plasma autoantibody levels [
3]. Molecular mimicry together with hyperactivity of the host’s immune system during the infection of COVID19 are some of the possible mechanisms for the induction of autoimmunity [
6]. One of the important features of the COVID-19 infection is elevated neutrophil-to-lymphocyte ratio and elevated neutrophil extracellular trap (NET) circulation. NETs, on the other hand, can further activate complement pathways causing tissue destruction and vasculitis [
7]. …