| First Author | Liu D | Year | 2022 |
| Journal | Science | Volume | 375 |
| Issue | 6581 | Pages | eabi5965 |
| PubMed ID | 35143305 | Mgi Jnum | J:324874 |
| Mgi Id | MGI:6867097 | Doi | 10.1126/science.abi5965 |
| Citation | Liu D, et al. (2022) CD97 promotes spleen dendritic cell homeostasis through the mechanosensing of red blood cells. Science 375(6581):eabi5965 |
| abstractText | Dendritic cells (DCs) are crucial for initiating adaptive immune responses. However, the factors that control DC positioning and homeostasis are incompletely understood. We found that type-2 conventional DCs (cDC2s) in the spleen depend on Galpha13 and adhesion G protein-coupled receptor family member-E5 (Adgre5, or CD97) for positioning in blood-exposed locations. CD97 function required its autoproteolytic cleavage. CD55 is a CD97 ligand, and cDC2 interaction with CD55-expressing red blood cells (RBCs) under shear stress conditions caused extraction of the regulatory CD97 N-terminal fragment. Deficiency in CD55-CD97 signaling led to loss of splenic cDC2s into the circulation and defective lymphocyte responses to blood-borne antigens. Thus, CD97 mechanosensing of RBCs establishes a migration and gene expression program that optimizes the antigen capture and presentation functions of splenic cDC2s. |
