A novel role for CD55 in granulocyte homeostasis and anti-bacterial host defense.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 21984892.
- Also identified by DOI 10.1371/journal.pone.0024431 and PMC identifier PMC2959053.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
BACKGROUND: In addition to its complement-regulating activity, CD55 is a ligand of the adhesion class G protein-coupled receptor CD97; however, the relevance of this interaction has remained elusive. We previously showed that mice lacking a functional CD97 gene have increased numbers of granulocytes. METHODOLOGY/RESULTS: Here, we demonstrate that CD55-deficient mice display a comparable phenotype with about two-fold more circulating granulocytes in the blood stream, the marginated pool, and the spleen. This granulocytosis was independent of increased complement activity. Augmented numbers of Gr-1-positive cells in cell cycle in the bone marrow indicated a higher granulopoietic activity in mice lacking either CD55 or CD97. Concomitant with the increase in blood granulocyte numbers, Cd55⁻/⁻ mice challenged with the respiratory pathogen Streptococcus pneumoniae developed less bacteremia and died later after infection. CONCLUSIONS: Collectively, these data suggest that complement-independent interaction of CD55 with CD97 is functionally relevant and involved in granulocyte homeostasis and host defense.