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Tafazzin (Taz) deficiency in BTHS patients results in an increased risk of infections. Mesenchymal stem cells (MSCs) are well known for their immune\u2010inhibitory function. We examined how Taz\u2010deficiency in murine MSCs impact their ability to modulate the function of lipopolysaccharide (LPS)\u2010activated wild type (WT) B lymphocytes. MSCs from tafazzin knockdown (TazKD) mice exhibited a reduction in mitochondrial cardiolipin compared to wild type (WT) MSCs. However, mitochondrial bioenergetics and membrane potential were unaltered. In contrast, TazKD MSCs exhibited increased reactive oxygen species generation and increased glycolysis. The increased glycolysis was associated with an elevated proliferation, phosphatidylinositol\u20103\u2010kinase expression and expression of the immunosuppressive markers indoleamine\u20102,3\u2010dioxygenase, cytotoxic T\u2010lymphocyte\u2010associated protein 4, interleukin\u201010, and cluster of differentiation 59 compared to controls. Inhibition of glycolysis with 2\u2010deoxyglucose attenuated the TazKD\u2010mediated increased expression of cytotoxic T\u2010lymphocyte\u2010associated protein 4 and interleukin\u201010. When co\u2010cultured with LPS\u2010activated WT B cells, TazKD MSCs inhibited B cell proliferation and growth rate and reduced B cell secretion of immunoglobulin M compared to controls. In addition, co\u2010culture of LPS\u2010activated WT B cells with TazKD MSCs promoted B cell differentiation toward interleukin\u201010 secreting plasma cells and B regulatory cells compared to controls. The results indicate that Taz deficiency in MSCs promote reprogramming of activated B lymphocytes toward immunosuppressive phenotypes.<\/jats:p>","DOI":"10.1096\/fj.202200145r","type":"journal-article","created":{"date-parts":[[2022,7,11]],"date-time":"2022-07-11T11:04:15Z","timestamp":1657537455000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Tafazzin deficiency in mouse mesenchymal stem cells promote reprogramming of activated B lymphocytes toward immunosuppressive phenotypes"],"prefix":"10.1096","volume":"36","author":[{"given":"Hana M.","family":"Zegallai","sequence":"first","affiliation":[{"name":"Diabetes Research Envisioned and Accomplished in Manitoba (DREAM) Theme, Children's Hospital Research Institute of Manitoba, Department of Pharmacology &amp; Therapeutics, Rady Faculty of Health Sciences University of Manitoba  Winnipeg Manitoba 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