Meta‐analysis confirmed genetic susceptibility conferred by multiple risk variants from CTLA4 and SERPINA1 in granulomatosis with polyangiitis

Abstract

Background: Granulomatosis with polyangiitis (GPA) is a rare systemic autoimmune disease. Smaller sample size and complex nature of the disease pathogenesis has made it challenging to perform well-powered genetic investigations. We performed a systematic review based meta-analysis in GPA to investigate the genetic susceptibility conferred by non-human leukocyte antigen (non-HLA) candidate genes.

Discovery of a shared therapeutic target in granulomatosis with polyangiitis and gastric tumor microenvironment

“…We found Banerjee et al's 1 report on the pathogenesis and complexity of granulomatous polyangiitis (GPA) to be intriguing. Through a strong genetic study, the authors were able to identify promising genes associated with the disease, including CTLA4 , PRTN3 , SERPINA1 , and PTPN22 .…”

Granulomatosis with polyangiitis with salivary glands involvement: Presenting a case and describing its clinical, pathophysiological, and therapeutic aspects

“…Also, via interaction between ANCA and PR3 enzyme, the adhesion of neutrophils to vascular endothelium can be triggered which leads to damage to endothelial cells 10 . Moreover, the over‐expression of some genes has been also described to be associated with GPA such as the CTLA‐4 gene (involves in T‐cell activation), PRTN‐3 (involves in activation of PR3), and HLA‐DP gene (involves in activation of neutrophils and monocytes) 11 . Regarding the etiologic role of infections, some evidence is available in the flaring role of hepatitis C virus, Epstein–Barr virus, cytomegalovirus, parvovirus, and COVID‐19 infections and the appearance of GPA 12,13 .…”

“… 10 Moreover, the over‐expression of some genes has been also described to be associated with GPA such as the CTLA‐4 gene (involves in T‐cell activation), PRTN‐3 (involves in activation of PR3), and HLA‐DP gene (involves in activation of neutrophils and monocytes). 11 Regarding the etiologic role of infections, some evidence is available in the flaring role of hepatitis C virus, Epstein–Barr virus, cytomegalovirus, parvovirus, and COVID‐19 infections and the appearance of GPA. 12 , 13 Also, it is now suggested a close link between the likelihood of GPA and some medications such as phenytoin, hydralazine, allopurinol, and anti‐thyroid drugs with unclear etiological roles.…”

Granulomatosis with polyangiitis with salivary glands involvement: presenting a case and describing its clinical, pathophysiological, and therapeutic aspects

“…Also, via interaction between ANCA and proteinase-3 enzyme, the adhesion of neutrophils to vascular endothelium can be triggered which leads to damage to endothelial cells (10). Moreover, the over-expression of some genes has been also described to be associated with GPA such as the CTLA-4 gene (involves in T-cells activation), PRTN-3 (involves in activation of proteinase-3), and HLA-DP gene (involves in activation of neutrophils and monocytes) (11). Regarding the etiologic role of infections, some evidence is available in the flaring role of hepatitis C virus, Epstein-Barr virus, cytomegalovirus, parvovirus, and Covid-19 infections and the appearance of GPA (12,13).…”