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Contributor
Benjamin T. Enslow
Digital Publisher
Digital Commons at St. Mary's University
Publication Date
Spring 2025
Keywords
Chronic inflammation; B cells; Nucleic acid antigen; CD36 expression
Description
In states of chronic inflammation, a subset of B cells exquisitely responsive to nucleic acid antigen and expressing the proinflammatory transcription factor T-bet have been found to accumulate1. Depending on the context, these T-bet+ B cells can play both protective and pathogenic roles, from enhancing antiviral defenses to contributing to autoreactive antibody production and exacerbating metabolic disease1,2.
• Recently, our laboratory and others have found that T-bet+ B cells extracted from human or murine tissues exhibit unusually high expression of the class B scavenger receptor and fatty acid translocase CD36.
• As CD36 expression in B cells is generally limited to specific subsets3,4, its presence on these T-bet+ B cells raises questions about its role in promoting pathogenic B cell responses.
• Here, we used flow cytometry to investigate if deletion of CD36 from B cells hindered T-bet B cell formation in R848 and HFD models.
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1 page
City
San Antonio, Texas
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.