Abstract
B cells are central players in multiple autoimmune rheumatic diseases as a result of the imbalance between pathogenic and protective B-cell functions, which are presumably mediated by distinct populations. Yet the functional role of different B-cell populations and the contribution of specific subsets to disease pathogenesis remain to be fully understood owing to a large extent to the use of pauci-color flow cytometry. Despite its limitations, this approach has been instrumental in providing a global picture of multiple B-cell abnormalities in multiple human rheumatic diseases, more prominently systemic lupus erythematosus, rheumatoid arthritis and Sjogren’s syndrome. Accordingly, these studies represent the focus of this review. In addition, we also discuss the added value of tapping into the potential of polychromatic flow cytometry to unravel a higher level of B-cell heterogeneity, provide a more nuanced view of B-cell abnormalities in disease and create the foundation for a precise understanding of functional division of labor among the different phenotypic subsets. State-of-the-art polychromatic flow cytometry and novel multidimensional analytical approaches hold tremendous promise for our understanding of disease pathogenesis, the generation of disease biomarkers, patient stratification and personalized therapeutic approaches.
Highlights
B cells play a central role in the pathogenesis of autoimmune diseases through a combination of antibodydependent and antibody-independent mechanisms
We present the current knowledge of human B-cell subsets and their analysis in rheumatic diseases using flow cytometry
Flow cytometry has emerged as a powerful tool for B-cell immunophenotyping through the use of increasing number of markers, as well as the incorporation of intracellular staining to interrogate the functional properties such as the production of cytokines and phosphorylation of key signaling molecules [2,87,94,95,96]
Summary
B cells play a central role in the pathogenesis of autoimmune diseases through a combination of antibodydependent and antibody-independent mechanisms. DN B cells resemble a tissue-based memory population phenotypically, but they do not express the characteristic FcRL4 cell surface marker in the peripheral blood of both healthy and SLE subjects [12]. A population of human peripheral blood B cells with a CD20+IgD+CD27+CD43+CD70− phenotype has been shown to exhibit the functional hallmarks of the mouse B1 cells [28], its actual significance and magnitude remain to be further explored.
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