AI Article Synopsis
- Dendritic cells (DCs), specifically type-2 conventional DCs (cDC2s), play a key role in starting adaptive immune responses, but how they are positioned and maintained in the spleen is not fully understood.
- The study highlights that cDC2s rely on a protein called CD97, which requires a specific modification (autoproteolytic cleavage) for correct positioning within the spleen.
- The interaction between cDC2s and red blood cells (RBCs) via CD55 under certain conditions leads to important changes in the DCs, and disruptions in this signaling pathway result in decreased cDC2s in the spleen and poorer immune responses to blood-borne pathogens.
Article Abstract
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 Gα 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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9310086 | PMC |
| http://dx.doi.org/10.1126/science.abi5965 | DOI Listing |
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