{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Aaron T"],"funding":["NIAID NIH HHS","NHLBI NIH HHS","Albert Einstein Cancer Center","HHS | NIH | National Institute of Allergy and Infectious Diseases","HHS | NIH | National Heart, Lung, and Blood Institute","NCI NIH HHS"],"pagination":["595-608"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9998356"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["210(5)"],"pubmed_abstract":["Both infection and autoimmune disease can disrupt pre-existing Ab titers leading to diminished serological memory, yet the underlying mechanisms are not well understood. In this article, we report that TNF-α, an inflammatory cytokine, is a master regulator of the plasma cell (PC) niche in the bone marrow (BM). Acute rTNF-α treatment depletes previously existing Ab titers after vaccination by limiting PC occupancy or retention in the BM. Consistent with this phenomenon, mice lacking TNF-α signaling have elevated PC capacity in the BM and higher Ab titers. Using BM chimeric mice, we found that PC egress from the BM is regulated in a cell-extrinsic manner, by radiation-resistant cells via TNF-α receptor 1 signaling, leading to increased vascular permeability and CD138 downregulation on PCs. P"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["TNF-α Limits Serological Memory by Disrupting the Bone Marrow Niche."],"pmcid":["PMC9998356"],"funding_grant_id":["R01 AI132633","F32 HL149155","P30 CA013330","R01AI132633","R01HL141491","R01 HL141491","P30CA013330","R01 HL152637","F32HL149155"],"pubmed_authors":["Aaron T","Ovando LJ","Chandran K","Benet Z","Fooksman D","Laudermilch E"],"additional_accession":[]},"is_claimable":false,"name":"TNF-α Limits Serological Memory by Disrupting the Bone Marrow Niche.","description":"Both infection and autoimmune disease can disrupt pre-existing Ab titers leading to diminished serological memory, yet the underlying mechanisms are not well understood. In this article, we report that TNF-α, an inflammatory cytokine, is a master regulator of the plasma cell (PC) niche in the bone marrow (BM). Acute rTNF-α treatment depletes previously existing Ab titers after vaccination by limiting PC occupancy or retention in the BM. Consistent with this phenomenon, mice lacking TNF-α signaling have elevated PC capacity in the BM and higher Ab titers. Using BM chimeric mice, we found that PC egress from the BM is regulated in a cell-extrinsic manner, by radiation-resistant cells via TNF-α receptor 1 signaling, leading to increased vascular permeability and CD138 downregulation on PCs. P","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Mar","modification":"2025-04-03T23:49:51.443Z","creation":"2025-04-03T23:49:51.443Z"},"accession":"S-EPMC9998356","cross_references":{"pubmed":["36645344"],"doi":["10.4049/jimmunol.2200053"]}}