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ABSTRACT: Background
Rituximab-mediated B-cell depletion in pemphigus patients is majorly caused by antibody-dependent cellular cytotoxicity. This is mediated by Fcγ receptors on immune cells, particularly FcγRIIIa (CD16) on natural killer (NK) cells. This study investigates the impact of FcγRIII expression on response to rituximab in pemphigus patients.Patients and methods
A cross-sectional study was carried out on 85 pemphigus patients who had been treated with rituximab using a rheumatoid arthritis protocol. Patients who achieved complete remission within 4.5 months were arbitrarily defined as responders. CD16 expression on NK cells, NK-T cells, and monocytes, as well as FcγRIIIa-158V/F polymorphism, were assessed using flow cytometry and genetic assays, respectively.Results</
SUBMITTER: Sharma A
PROVIDER: S-EPMC12270442 | biostudies-literature | 2025 Jul-Aug
REPOSITORIES: biostudies-literature