ArticleDisease models & mechanisms2015
Cx3cr1 deficiency in mice attenuates hepatic granuloma formation during acute schistosomiasis by enhancing the M2-type polarization of macrophages.
Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- CX3CL1/CX3CR1 axis in liver disease: context-dependent roles and balance.Frontiers in immunology · 2026Review
- Prognostic assessment of early-stage liver cirrhosis induced by HCV using an integrated model of CX3CR1-associated immune infiltration genes.Scientific reports · 2025Article
- Exosomal PPARγ derived from macrophages suppresses LPS-induced peritonitis by negative regulation of CD14/TLR4 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- 5-aminolevulinate and CHIL3/CHI3L1 treatment amid ischemia aids liver metabolism and reduces ischemia-reperfusion injury.Theranostics · 2023Article
- CX3CR1-Expressing Myeloid Cells Regulate Host-Helminth Interaction and Lung Inflammation.Advanced biology · 2022Article
- C-X3-C motif chemokine ligand 1/receptor 1 regulates the M1 polarization and chemotaxis of macrophages after hypoxia/reoxygenation injury.Chronic diseases and translational medicine · 2021Article
- Kdm2a deficiency in macrophages enhances thermogenesis to protect mice against HFD-induced obesity by enhancing H3K36me2 at the Pparg locus.Cell death and differentiation · 2021Article
- PPAR Gamma: From Definition to Molecular Targets and Therapy of Lung Diseases.International journal of molecular sciences · 2021Review
- Targeted Inhibition of FTO Demethylase Protects Mice Against LPS-Induced Septic Shock by Suppressing NLRP3 Inflammasome.Frontiers in immunology · 2021Article
- Association of CX3CL1 and CX3CR1 Expression with Liver Fibrosis in a Mouse Model of Schistosomiasis.Current medical science · 2020Article
- P21 activated kinase-1 (PAK1) in macrophages is required for promotion of Th17 cell response during helminth infection.Journal of cellular and molecular medicine · 2020Article
- Mycobacterium tuberculosis Heat-Shock Protein 16.3 Induces Macrophage M2 Polarization Through CCRL2/CX3CR1.Inflammation · 2020Article
- Blockade of JAK2 protects mice against hypoxia-induced pulmonary arterial hypertension by repressing pulmonary arterial smooth muscle cell proliferation.Cell proliferation · 2020Article
- Monocyte and Macrophage-Mediated Pathology and Protective Immunity During Schistosomiasis.Frontiers in microbiology · 2020Review
- C/EBP Homologous Protein (CHOP) Activates Macrophages and Promotes Liver Fibrosis inJournal of immunology research · 2019Article
- Loss of Jak2 protects cardiac allografts from chronic rejection by attenuating Th1 response along with increased regulatory T cells.American journal of translational research · 2019Article
- Indispensable Role of CXFrontiers in immunology · 2019Article
- Both conditional ablation and overexpression of E2 SUMO-conjugating enzyme (UBC9) in mouse pancreatic beta cells result in impaired beta cell function.Diabetologia · 2018Article
- Hematopoietic MyD88 and IL-18 are essential for IFN-γ-dependent restriction of type AJournal of leukocyte biology · 2017Article
- Chop Deficiency Protects Mice Against Bleomycin-induced Pulmonary Fibrosis by Attenuating M2 Macrophage Production.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute schistosomiasis is characterized by pro-inflammatory responses against tissue- or organ-trapped parasite eggs along with granuloma formation. Here, we describe studies in Cx3cr1(-/-) mice and demonstrate the role of Cx3cr1 in the pathoetiology of granuloma formation during acute schistosomiasis. Mice deficient in Cx3cr1 were protected from granuloma formation and hepatic injury induced by Schistosoma japonicum eggs, as manifested by reduced body weight loss and attenuated hepatomegaly along with preserved liver function. Notably, S. japonicum infection induced high levels of hepatic Cx3cr1 expression, which was predominantly expressed by infiltrating macrophages. Loss of Cx3cr1 rendered macrophages preferentially towards M2 polarization, which then led to a characteristic switch of the host immune defense from a conventional Th1 to a typical Th2 response during acute schistosomiasis. This immune switch caused by Cx3cr1 deficiency was probably associated with enhanced STAT6/PPAR-γ signaling and increased expression of indoleamine 2,3-dioxygenase (IDO), an enzyme that promotes M2 polarization of macrophages. Taken together, our data provide evidence suggesting that CX3CR1 could be a viable therapeutic target for treatment of acute schistosomiasis.
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