ArticleBlood2005
CXCL9 inhibits eosinophil responses by a CCR3- and Rac2-dependent mechanism.
Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 47 citations in OpenAlex.
- Eosinophil biology in COPD: from scientific insight to clinical treatment action.ERJ open research · 2026Review
- TLR7/8 signaling activation enhances the potency of human pluripotent stem cell-derived eosinophils in cancer immunotherapy for solid tumors.Experimental hematology & oncology · 2025Article
- Origins and functions of eosinophils in two non-mucosal tissues.Frontiers in immunology · 2024Review
- Cellular Context Dictates the Suppression or Augmentation of Triple-Negative Mammary Tumor Metastasis by NLRX1.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Eosinophil: An innate immune cell with anti-filarial vaccine and biomarker potential.Health science reports · 2023Article
- Aiolos regulates eosinophil migration into tissues.Mucosal immunology · 2021Article
- Analysis of the signal cross talk via CCL26 in the tumor microenvironment in osteosarcoma.Scientific reports · 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
- Microbial Regulation of Enteric Eosinophils and Its Impact on Tissue Remodeling and Th2 Immunity.Frontiers in immunology · 2020Article
- Rho and Rac, but not ROCK, are required for secretion of human and mouse eosinophil-associated RNases.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2019Article
- Involvement and Possible Role of Eosinophils in Asthma Exacerbation.Frontiers in immunology · 2018Review
- Characteristics of Allergic Pulmonary Inflammation in CXCR3Knockout Mice Sensitized and Challenged with House Dust Mite Protein.PloS one · 2016Article
- Modulation of Chemokine Responses: Synergy and Cooperativity.Frontiers in immunology · 2016Review
- STAT1 signaling is essential for protection against Cryptococcus neoformans infection in mice.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Actin cytoskeletal defects in immunodeficiency.Immunological reviews · 2013Review
- Up-regulation of chemokine C-C ligand 2 (CCL2) and C-X-C chemokine 8 (CXCL8) expression by monocytes in chronic idiopathic urticaria.Clinical and experimental immunology · 2012Article
- Agonist activation of f-actin-mediated eosinophil shape change and mediator release is dependent on Rac2.International archives of allergy and immunology · 2011Article
- Rho GTPases in hematopoiesis and hemopathies.Blood · 2010Review
- Aberrant inflammatory response to Streptococcus pyogenes in mice lacking myeloid differentiation factor 88.The American journal of pathology · 2010Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Recently, inhibitory cytokine pathways for leukocyte chemoattraction and activation have been identified, but there is little insight into the operational mechanisms except for models that rely on simple receptor antagonism. We have previously identified the existence of a murine eosinophil inhibitory pathway mediated by the CXC chemokine ligand 9 (CXCL9, Mig [monokine induced by interferon-gamma]) that impressively blocks eosinophil chemoattraction and function, but the mechanism has remained elusive. We now demonstrate that Mig's inhibitory action extends beyond receptor antagonism alone. Notably, in addition to inhibiting eotaxin-induced filamentous actin (F-actin) formation and chemoattraction, Mig potently blocks platelet activating factor (PAF)- and leukotriene B4 (LTB4)-induced responses. Remarkably, Mig-treated eosinophils display an abnormal F-actin assembly in the absence of agonist stimulation. Additionally, Mig pretreatment inhibits eotaxin-induced activation of the Rho-guanosine triphosphatase (GTPase) Rac, and Rac2-deficient eosinophils demonstrate an impaired transmigration and actin polymerization response to eotaxin stimulation. Furthermore, Mig was unable to inhibit eotaxin-induced responses in Rac2-deficient eosinophils. Finally, using CCR3 gene-targeted cells, Mig's inhibitory activity is demonstrated to be mediated by CC chemokine receptor 3 (CCR3). Thus, by altering agonist-induced signaling and abrogating cytoskeletal reorganization by a Rac2-dependent mechanism, Mig markedly inhibits eosinophil responses to diverse stimuli. These results establish evidence that distinct chemokines can use CCR3 to induce opposing signals in eosinophils.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.