Mechanistic basis for impaired B cell depletion after anti-CD20 treatment of African American with neuro-inflammatory disorders

Brief description of study

Infusable anti-CD20 (aCD20) therapies (rituximab, ocrelizumab) emerged as the mainstay of treatment in multiple sclerosis and related disorders (MSARD). Standard, every-6-month dosing of aCD20 achieves complete blood B-cell depletion in 99% of patients. However, some patients do not have complete B-cell depletion, which we postulate results from genetic polymorphisms influencing antibody-dependent cell cytotoxicity, complement-dependent pathways, or other factors. To unravel the mechanistic basis for early B-cell repletion, we will perform in-depth microfluorometric analyses of blood samples, BAFF cytokine measurement, and also study genetic polymorphisms relevant to B-cell biology using comprehensive Illumina genetic chip. Identification of mechanism(s) responsible for accelerated repletion, which may reflect suboptimal treatment, may enhance our understanding of how B-cell depletion is achieved with aCD20 therapies, and lead to personalized treatment regimens.

Clinical Study Identifier: s22-00483

Principal Investigator: Ilya Kister.

Other Investigators: Carrie Lyn Sammarco, Arnaldo A Arbini, Michelle Krogsgaard, Gregg Silverman, Tyler Ellis Smith, Vito Pasquale Arena, David Fenyo, Jonathan E Howard, Jennifer K Abate, Robert W Charlson, Lauren B. Krupp.

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