In Vitro Characterization of Human CD24hiCD38hi Regulatory B Cells Shows CD9 Is Not a Stable Breg Cell Marker |
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Authors: | Fatin N Mohd Jaya Sergio G Garcia Francesc E Borras Dolores Guerrero Godfrey C F Chan Marcella Franquesa |
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Affiliation: | 1.School of Biomedical Sciences, Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Hong Kong, China;2.REMAR-IVECAT Group, Health Science Research Institute Germans Trias i Pujol, Can Ruti Campus, 08916 Badalona, Spain; (S.G.G.); (F.E.B.);3.Otorhinolaryngology Department, Hospital Universitari Germans Trias i Pujol, 08916 Badalona, Spain;4.Department of Pediatrics and Adolescent Medicine, Faculty of Medicine, The University of Hong Kong, 21 Sassoon Road, Hong Kong, China; |
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Abstract: | Regulatory B (Breg) cells are endowed with immune suppressive functions. Various human and murine Breg subtypes have been reported. While interleukin (IL)-10 intracellular staining remains the most reliable way to identify Breg cells, this technique hinders further essential functional studies. Recent findings suggest that CD9 is an effective surface marker of murine IL-10 competent Breg cells. However, the stability of CD9 and its relevance as a unique marker for human Breg cells, which have been widely characterized as CD24hiCD38hi, have not been investigated. Here, we demonstrate that CD9 expression is sensitive to in vitro B cell stimulations. CD9 expression could either be re-expressed or downregulated in purified CD9-negative B cells and CD9-positive B cells, respectively. We found no significant differences in the Breg differentiation capacity of the CD9-negative and CD9-positive B cells. Furthermore, CD9-positive B cells co-express CD40 and CD86, suggesting their nature as B cell activation or co-stimulatory molecules, rather than regulatory ones. Therefore, we report the relatively unstable CD9 as a distinct surface molecule, indicating the need for further research for a more reliable marker to purify human Breg cells. |
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Keywords: | CD9 regulatory B cells immune tolerance immune homeostasis inflammation |
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