| Literature DB >> 35236754 |
Ying Ying Yiu1,2, Paige S Hansen1,3, Laughing Bear Torrez Dulgeroff1, Grace Blacker1, Lara Myers4, Sarah Galloway1, Eric Gars5, Olivia Colace1, Paul Mansfield1, Kim J Hasenkrug4, Irving L Weissman6,5,7,8, Michal Caspi Tal6,3.
Abstract
CD47 is an important innate immune checkpoint through its interaction with its inhibitory receptor on macrophages, signal-regulatory protein α (SIRPα). Therapeutic blockade of CD47-SIRPα interactions is a promising immuno-oncology treatment that promotes clearance of cancer cells. However, CD47-SIRPα interactions also maintain homeostatic lymphocyte levels. In this study, we report that the mouse splenic marginal zone B cell population is dependent on intact CD47-SIRPα interactions and blockade of CD47 leads to the loss of these cells. This depletion is accompanied by elevated levels of monocyte-recruiting chemokines CCL2 and CCL7 and infiltration of CCR2+Ly6Chi monocytes into the mouse spleen. In the absence of CCR2 signaling, there is no infiltration and reduced marginal zone B cell depletion. These data suggest that CD47 blockade leads to clearance of splenic marginal zone B cells.Entities:
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Year: 2022 PMID: 35236754 PMCID: PMC9012117 DOI: 10.4049/jimmunol.2100352
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.426