{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chakraborty M"],"funding":["NIAID NIH HHS","NHLBI NIH HHS","HHS | NIH | National Institute of Allergy and Infectious Diseases","NIGMS NIH HHS"],"pagination":["1075-1080"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10948292"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["212(7)"],"pubmed_abstract":["B cell trafficking involves the coordinated activity of multiple adhesive and cytokine-receptor interactions, and the players in this process are not fully understood. In this study, we identified the tetraspanin CD53 as a critical regulator of both normal and malignant B cell trafficking. CXCL12 is a key chemokine in B cell homing to the bone marrow and secondary lymphoid organs, and both normal and malignant B cells from Cd53-/- mice have reduced migration toward CXCL12 in vitro, as well as impaired marrow homing in vivo. Using proximity ligation studies, we identified the CXCL12 receptor, CXCR4, as a novel, to our knowledge, CD53 binding partner. This interaction promotes receptor function, because Cd53-/- B cells display reduced signaling and internalization of CXCR4 in response to CXCL12. Together, our data suggest that CD53 interacts with CXCR4 on both normal and malignant B cells to promote CXCL12 signaling, receptor internalization, and marrow homing."],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["Cutting Edge: The Tetraspanin CD53 Promotes CXCR4 Signaling and Bone Marrow Homing in B Cells."],"pmcid":["PMC10948292"],"funding_grant_id":["R01 HL134896","T32 GM007067","R01 AI173077","R01 AI158500"],"pubmed_authors":["Li W","Roundy N","Duncavage E","Bednarski JJ","Paracatu LC","Schuettpelz LG","Greenberg ZJ","Dong Q","Chakraborty M"],"additional_accession":[]},"is_claimable":false,"name":"Cutting Edge: The Tetraspanin CD53 Promotes CXCR4 Signaling and Bone Marrow Homing in B Cells.","description":"B cell trafficking involves the coordinated activity of multiple adhesive and cytokine-receptor interactions, and the players in this process are not fully understood. In this study, we identified the tetraspanin CD53 as a critical regulator of both normal and malignant B cell trafficking. CXCL12 is a key chemokine in B cell homing to the bone marrow and secondary lymphoid organs, and both normal and malignant B cells from Cd53-/- mice have reduced migration toward CXCL12 in vitro, as well as impaired marrow homing in vivo. Using proximity ligation studies, we identified the CXCL12 receptor, CXCR4, as a novel, to our knowledge, CD53 binding partner. This interaction promotes receptor function, because Cd53-/- B cells display reduced signaling and internalization of CXCR4 in response to CXCL12. Together, our data suggest that CD53 interacts with CXCR4 on both normal and malignant B cells to promote CXCL12 signaling, receptor internalization, and marrow homing.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Apr","modification":"2025-07-02T03:04:15.18Z","creation":"2025-07-02T03:04:15.18Z"},"accession":"S-EPMC10948292","cross_references":{"pubmed":["38363205"],"doi":["10.4049/jimmunol.2300336"]}}