Commensal bacteria contribute to insulin resistance in aging by activating innate B1a cells
Monica Bodogai(National Institute on Aging), Jennifer O’Connell(National Institute on Aging), Ki H. Kim(National Institute on Aging), Yoo Kim(National Institute on Aging), Kanako Moritoh(National Institute on Aging), Chen Chen(National Institute on Aging), Fedor Gusev(Vavilov Institute of General Genetics), Kelli L. Vaughan(National Institute on Aging), Natalia Shulzhenko(Oregon State University), Julie A. Mattison(National Institute on Aging), Catalina Lee-Chang(University of Massachusetts Chan Medical School), Weixuan Chen(Janssen (Belgium)), Olga D. Carlson(National Institute on Aging), Kevin G. Becker(National Institute on Aging), Manoj Gurung(Oregon State University), Andrey Morgun(Oregon State University), James R. White(Resphera Biosciences), Theresa Meade(National Institute on Aging), Kathy A Perdue(National Institute on Aging), Matthias Mack(University Hospital Regensburg), Luigi Ferrucci(National Institute on Aging), Giorgio Trinchieri(Frederick National Laboratory for Cancer Research), Rafael de Cabo(National Institute on Aging), Е. И. Рогаев(University of Massachusetts Chan Medical School), Josephine M. Egan(National Institute on Aging), Jiejun Wu(Janssen (Belgium)), Arya Biragyn(National Institute on Aging)
Cited by 181Open Access
Abstract
monocytes or 4BL cells had the same effect on IR. These results underscore the pathological function of B1a cells and suggest that the microbiome-monocyte-B cell axis could potentially be targeted to reverse age-associated IR.
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