ArticleJournal of leukocyte biology2020
Frontline Science: Antagonism between regular and atypical Cxcr3 receptors regulates macrophage migration during infection and injury in zebrafish.
Article in Journal of leukocyte biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Protective versus deleterious roles of pyroptosis in Mycobacterium avium and Mycobacterium marinum infections.Cell death & disease · 2026Article
- Temporal dynamics of macrophage transcriptional profiles during zebrafish wound healing.Frontiers in immunology · 2025Article
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- Expression and regulation of the CXCL9-11 chemokines and CXCR3 receptor in Atlantic salmonFrontiers in immunology · 2024Article
- Direct male development in chromosomally ZZ zebrafish.Frontiers in cell and developmental biology · 2024Article
- The regenerative response of cardiac interstitial cells.Journal of molecular cell biology · 2023Article
- Molecular Actors of Inflammation and Their Signaling Pathways: Mechanistic Insights from Zebrafish.Biology · 2023Review
- CXCL9-11 chemokines and CXCR3 receptor in teleost fish species.Fish and shellfish immunology reports · 2022Review
- Convergent copy number increase of genes associated with freshwater colonization in fishes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Article
- Zebrafish: an underutilized tool for discovery in host-microbe interactions.Trends in immunology · 2022Review
- Global gene expression responses of Atlantic salmon skin to Moritella viscosa.Scientific reports · 2022Article
- A fresh look at mycobacterial pathogenicity with the zebrafish host model.Molecular microbiology · 2022Review
- The Extended N-Terminal Domain Confers Atypical Chemokine Receptor Properties to CXCR3-B.Frontiers in immunology · 2022Article
- Evolution, Expression and Functional Analysis of CXCR3 in Neuronal and Cardiovascular Diseases: A Narrative Review.Frontiers in cell and developmental biology · 2022Review
- A Novel Function of TLR2 and MyD88 in the Regulation of Leukocyte Cell Migration Behavior During Wounding in Zebrafish Larvae.Frontiers in cell and developmental biology · 2021Article
- Glucocorticoid-Induced Exacerbation of Mycobacterial Infection Is Associated With a Reduced Phagocytic Capacity of Macrophages.Frontiers in immunology · 2021Article
- Cxcl9l and Cxcr3.2 regulate recruitment of osteoclast progenitors to bone matrix in a medaka osteoporosis model.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Frontline Science: Antagonism between regular and atypical Cxcr3 receptors regulates macrophage migration during infection and injury in zebrafish.Journal of leukocyte biology · 2020Article
- Macrophage ACKRobatics: An atypical Cxcr3 keeps macrophages in check.Journal of leukocyte biology · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CXCR3-CXCL11 chemokine-signaling axis plays an essential role in infection and inflammation by orchestrating leukocyte trafficking in human and animal models, including zebrafish. Atypical chemokine receptors (ACKRs) play a fundamental regulatory function in signaling networks by shaping chemokine gradients through their ligand scavenging function, while being unable to signal in the classic G-protein-dependent manner. Two copies of the CXCR3 gene in zebrafish, cxcr3.2 and cxcr3.3, are expressed on macrophages and share a highly conserved ligand-binding site. However, Cxcr3.3 has structural characteristics of ACKRs indicative of a ligand-scavenging role. In contrast, we previously showed that Cxcr3.2 is an active CXCR3 receptor because it is required for macrophage motility and recruitment to sites of mycobacterial infection. In this study, we generated a cxcr3.3 CRISPR-mutant to functionally dissect the antagonistic interplay among the cxcr3 paralogs in the immune response. We observed that cxcr3.3 mutants are more susceptible to mycobacterial infection, whereas cxcr3.2 mutants are more resistant. Furthermore, macrophages in the cxcr3.3 mutant are more motile, show higher activation status, and are recruited more efficiently to sites of infection or injury. Our results suggest that Cxcr3.3 is an ACKR that regulates the activity of Cxcr3.2 by scavenging common ligands and that silencing the scavenging function of Cxcr3.3 results in an exacerbated Cxcr3.2 signaling. In human, splice variants of CXCR3 have antagonistic functions and CXCR3 ligands also interact with ACKRs. Therefore, in zebrafish, an analogous regulatory mechanism appears to have evolved after the cxcr3 gene duplication event, through diversification of conventional and atypical receptor variants.
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