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ORIGINAL ARTICLE
Year : 2019  |  Volume : 44  |  Issue : 1  |  Page : 54-64

Improperly functioning phagocytic cells contribute to disturbed phagocytosis in chronic lymphocytic leukaemia


1 Department of Clinical Pathology, Faculty of Medicine, Alexandria University Hospitals, Alexandria, Egypt
2 Hematology Unit, Department of Internal Medicine, Faculty of Medicine, Alexandria University Hospitals, Alexandria, Egypt

Correspondence Address:
Amira I Fayad
Department of Clinical Pathology, Faculty of Medicine, Alexandria University Hospitals, Al Khartoum Square, El Azareta, Alexandria, 21526
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejh.ejh_19_18

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Background Patients with chronic lymphocytic leukaemia (CLL) are endangered by fatal infectious complications. CLL cells shape their surrounding microenvironment as immune effectors which manifests as tolerance mechanisms, avoiding self-reactivity and inhibiting phagocytosis. Immune-therapeutic approaches tailoring antitumor potentials of phagocytic cells have been the focus of recent studies. Aim To study whether examining phagocytic cells’ functional status in patients with CLL can provide insights into immune system deregulation responsible for fatal infectious complications. Patients and methods The study was conducted on patients with CLL: 30 de-novo (group IA), 30 treated (group IB), and 20 healthy age-matched and sex-matched volunteers. Phagocytosis by neutrophils and monocytes was studied using phagotest kit, assayed as percentage of cells ingesting FITC-Escherichia coli, and phagocytosis mean fluorescence intensity (MFI), representing individual cellular phagocytic activity. Phagocytic activity was correlated with corresponding leukocytes CD47 surface expression levels. Results There was a decreased percentage of neutrophils and monocytes ingesting bacteria in subgroup IA or IB compared with group II (P=0.043 and 0.015, respectively). Phagocytosis MFI by neutrophils or monocytes in subgroup IA or IB was lower than control group. There was increased CD47 surface expression by lymphocytes, neutrophils, and monocytes at the time of diagnosis, which decreased as the disease progressed; however, it was still higher than the control group. Paradoxical correlation was detected between CD47 surface expression levels and phagocytosis MFI by neutrophils or monocytes (r2=0.606, P=0.02, and r2=−0.419, P=0.6, respectively). Conclusion In CLL, phagocytic cells were improperly functioning and the percentage of functioning cells was decreased. CD47 expression levels by leukocytes varied throughout the course of the disease, reflecting disease progression and paradoxically correlated with phagocytic function.


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