| Literature DB >> 28228257 |
Arielle Glatman Zaretsky1, Christoph Konradt1, Fabien Dépis2, James B Wing3, Radhika Goenka4, Daniela Gomez Atria4, Jonathan S Silver1, Sunglim Cho5, Amaya I Wolf6, William J Quinn4, Julie B Engiles1, Dorothy C Brown1, Daniel Beiting1, Jan Erikson6, David Allman4, Michael P Cancro4, Shimon Sakaguchi3, Li-Fan Lu5, Christophe O Benoist2, Christopher A Hunter7.
Abstract
Long-lived plasma cells (PCs) in the bone marrow (BM) are a critical source of antibodies after infection or vaccination, but questions remain about the factors that control PCs. We found that systemic infection alters the BM, greatly reducing PCs and regulatory T (Treg) cells, a population that contributes to immune privilege in the BM. The use of intravital imaging revealed that BM Treg cells display a distinct behavior characterized by sustained co-localization with PCs and CD11c-YFP+ cells. Gene expression profiling indicated that BM Treg cells express high levels of Treg effector molecules, and CTLA-4 deletion in these cells resulted in elevated PCs. Furthermore, preservation of Treg cells during systemic infection prevents PC loss, while Treg cell depletion in uninfected mice reduced PC populations. These studies suggest a role for Treg cells in PC biology and provide a potential target for the modulation of PCs during vaccine-induced humoral responses or autoimmunity.Entities:
Keywords: B cells; T regulatory cell; antibody; bone marrow; infectious disease; plasma cell
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Year: 2017 PMID: 28228257 PMCID: PMC5361408 DOI: 10.1016/j.celrep.2017.01.067
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423