biostudies-literatureUnknown12Bakri FGChronic granulomatous Disease (CGD) is a rare innate immunodeficiency disorder caused by mutations in one of the six genes (<i>CYBA, CYBB, NCF1, NCF2, NCF4</i>, and <i>CYBC1</i>/EROS) encoding the superoxide-producing nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase complex in phagocytes. In the Western population, the most prevalent form of CGD (about two-thirds of all cases) is the X-linked form (X-CGD) caused by mutations in <i>CYBB</i>. The autosomal recessive forms (AR-CGD), due to mutations in the other genes, collectively account for the remaining one-third of CGD cases. We investigated the clinical and molecular features of 22 Jordanian, 7 Libyan, and 2 Iraqi CGD patients from 21 different families. In addition, 11 sibling patients from these families were suspected to hFrontiers in immunology639226https://www.ebi.ac.uk/biostudies/studies/S-EPMC7973097biostudies-literatureSecond Report of Chronic Granulomatous Disease in Jordan: Clinical and Genetic Description of 31 Patients From 21 Different Families, Including Families From Lybia and Iraq.PMC7973097Rendu JAl-Wahadneh AMSarhan MMMollin MBakri FGAlzyoud RMVigne BAl-Ramahi JAWStasia MJShukair MEAFaure JHayajneh WARoux-Buisson NKaradshe MFDaoud AKBeaumel SfalseSecond Report of Chronic Granulomatous Disease in Jordan: Clinical and Genetic Description of 31 Patients From 21 Different Families, Including Families From Lybia and Iraq.Chronic granulomatous Disease (CGD) is a rare innate immunodeficiency disorder caused by mutations in one of the six genes (<i>CYBA, CYBB, NCF1, NCF2, NCF4</i>, and <i>CYBC1</i>/EROS) encoding the superoxide-producing nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase complex in phagocytes. In the Western population, the most prevalent form of CGD (about two-thirds of all cases) is the X-linked form (X-CGD) caused by mutations in <i>CYBB</i>. The autosomal recessive forms (AR-CGD), due to mutations in the other genes, collectively account for the remaining one-third of CGD cases. We investigated the clinical and molecular features of 22 Jordanian, 7 Libyan, and 2 Iraqi CGD patients from 21 different families. In addition, 11 sibling patients from these families were suspected to h2021-01-01T00:00:00Z20212025-04-22T08:18:12.649Z2024-12-04T06:31:49.563ZS-EPMC79730973374697910.3389/fimmu.2021.639226