Influence of CD16 (FcγRIII) Expression on Peripheral Blood Mononuclear Cells on Response to Treatment with Rituximab...

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.

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.

CD16 expression on NK cells and NK-T cells was higher in responders than in resistant patients but did not reach statistical significance. A significant negative correlation was observed between NK-T cell percentage and time to remission (P < 0.001), suggesting NK-T cell percentage as a possible marker for prediction of time to remission. Distribution of FcγRIIIa genotypes (V/V, V/F, F/F) did not significantly differ between responders and resistant patients (P = 0.574). A statistically non-significant trend suggested that FF homozygotes may have a slightly worse survival outcome in achieving remission compared to FV/VV genotypes, with a hazard ratio of 1.255 (95% CI: 0.6112-2.577).

Small, single-center sample, potential selection bias, and lack of long-term follow-up or functional assays.

This study underscores the potential influence of CD16 expression and FcγRIIIa polymorphism in response to rituximab in pemphigus patients, emphasizing the need for further research to establish definitive relationships for personalized treatment strategies.