Primary immunodeficiency disorder (PID) refers to a heterogeneous group of disorderscharacterized by poor or absent function in one or more components of the immune system.Chronic granulomatous disease (CGD) is a primary immunodeficiency disorder caused byinherited defects in the NADPH oxidase complex. CD27 is considered an immunophenotypicmarker identifying peripheral blood memory B cells. In humans, differentially spliced isoformsof the leukocyte common Ag (CD45) have been used to discriminate populations that werethought to represent naive and memory cells. CD45RA is expressed on naïve T cells, as well asthe effector cells in both CD4 and CD8. After antigen experience, central and effector memoryT cells gain expression of CD45RO and lose expression of CD45RA. The aim of the study was to identify the alteration in peripheral blood B and T cellcompartments in patients with CGD (to detect CD45RO versus CD45RA & to identify alterationin CD27 in CGD patients). Our study included 30 CGD patients (22 males and 8 females) with ages ranging from 40days to 16 years. Patients with CGD diagnosed by DHR test (dihydrorhodamine) together withthe clinical picture of the disease. Besides, our study included 30 age and sex matched healthycontrols, for comparison.Anticoagulated (EDTA) samples were stained using the whole blood lysis method. CD19was stained simultaneously with each of the other markers (CD27, CD45RO, CD45RA) andanalyzed by flow cytometry. The samples were stained with CD3 simultaneously with each ofthe other markers (CD27, CD45RO, CD45RA) and analyzed by flow cytometry. The absolute count of CD27+ B cells was lower in CGD patients than healthy controlgroup with no statistical significance and there was a statistical significant decrease in expressionof CD45RA on T-lymphocytes in CGD patients compared to the healthy control group. Patients with CGD had an altered adaptive immunity, characterized by reduction in totallymphocyte and profound reduction of CD27-positive memory B cells but an expansion of CD45RO-positive T cells on the expense of CD45RA.