Early studies investigating Alemtuzumab (Lemtrada) in multiple sclerosis (MS) patients suggested that depletion of CD27⁺ memory B cells was a possible mechanism of action. Whether other B cell subsets are affected by Alemtuzumab is not known and was investigated in this in-depth phenotypic analysis of B cell subsets within alemtuzumab-treated MS patients.

Alemtuzumab is a monoclonal antibody specific for CD52, which is expressed on mature lymphocytes. It is thought to work as a disease-modifying therapy in relapse-remitting MS by depleting autoreactive T and B cells.

Peripheral blood mononuclear cells from MS patients after long-term (2 years-post) alemtuzumab treatment were stained with our panel of 40 isotope-conjugated antibodies. Mass cytometry, which combines flow cytometry with mass spectrometry, was then used to analyse and phenotype B cell subsets with unparalleled depth.

Analysis of the mass cytometry data showed that long-term alemtuzumab-induced remission is associated with continuing low levels of CD27⁺ IgD^– switched and CD27⁺ IgD^– non-switched memory B cells 2 years-post initial treatment.

Mass cytometry revealed which B cell subsets are affected by alemtuzumab treatment after long periods of time. These studies will allow us to track efficacy and design new ways of targeting these B cells more specifically.