Psoriasis is an erythematous-squamous dermatosis with a polygenic inheritance history. Both environmental and genetic factors play a role in the etiology of the disease. Over the past two decades, numerous linkage analyzes and genome-wide association studies have been conducted to investigate the role of genetic variation in disease pathogenesis and progression. To date, >70 psoriasis susceptibility loci have been identified, including HLA-Cw6, IL12B, IL23R, and LCE3B/3C. Some genetic markers are used in clinical diagnosis, prognosis, treatment, and personalized new drug development that can further explain the pathogenesis of psoriasis. This review summarizes the immunological mechanisms involved in the etiopathogenesis of psoriasis and recent advances in susceptibility genes and highlights new potential targets for therapeutic intervention.

Background Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) are a group of small vessel vasculitides characterized by necrotizan vasculitis and inflammation. The phenotypes of AAV include microscopic polyangiitis (MPA), granulomatosis and polyangiitis (GPA), and eosinophilic granulomatosis and polyangiitis (EGPA). The pathogenesis of AAV is multifactorial, and it is suggested that both genetic and environmental factors can influence these disorders. Main body Several candidate gene studies and genome-wide association studies (GWAS) have been conducted to investigate the genetic associations with AAV in recent years. Numerous genes have been related to the pathogenesis of AAV, including the innate, adaptive immune system and coagulation systems. Conclusion This review summarizes the immunological mechanisms involved in the etiopathogenesis of AAV and recent advances in susceptibility genes.