Quantitative assessment of CD79B depletion as a biomarker of accelerated B cell progenitor aging.

We previously demonstrated that age-related dysfunction in lipid synthesis pathways is associated with impaired B cell progenitor development in mice and humans. Here, we describe an optimized protocol for the quantification of CD79B, a novel biomarker of accelerated aging identified in our multi-omics immune aging study. Flow cytometric analyses of immune cell subpopulations revealed selective depletion of CD19+CD79B+ lymphoid progenitors in bone marrow from aged mice and accelerated aging models, phenocopying advanced physiological aging in humans. Thus, this detailed protocol provides a validated platform to interrogate novel biomarkers of hematopoietic stem and progenitor cell dysfunction associated with systemic aging.