ArticlePLoS pathogens2009
Retnla (relmalpha/fizz1) suppresses helminth-induced Th2-type immunity.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers.
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Who cites it
149 citing papers in PubMed, 213 citations in OpenAlex.
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- Helminth infection induces RELMα-dependent adipose tissue transcriptional reprogramming and protection against diet-induced obesity.bioRxiv : the preprint server for biology · 2026Article
- Influenza-induced tuft cell expansion alters ILC-mediated inflammation.bioRxiv : the preprint server for biology · 2026Article
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- Circadian rhythms of macrophages are altered by the acidic tumor microenvironment.EMBO reports · 2024Article
- Monocyte-macrophages modulate intestinal homeostasis in inflammatory bowel disease.Biomarker research · 2024Review
- Choline metabolism underpins macrophage IL-4 polarization and RELMα up-regulation in helminth infection.PLoS pathogens · 2023Article
- Resistin-like Molecule α and Pulmonary Vascular Remodeling: A Multi-Strain Murine Model of Antigen and Urban Ambient Particulate Matter Co-Exposure.International journal of molecular sciences · 2023Article
- Pulmonary inflammation promoted by type-2 dendritic cells is a feature of human and murine schistosomiasis.Nature communications · 2023Article
- Immunological mechanisms involved in macrophage activation and polarization in schistosomiasis.Parasitology · 2023Review
- Th2-dependent STAT6-regulated genes in intestinal epithelial cells mediate larval trapping during secondary Heligmosomoides polygyrus bakeri infection.PLoS pathogens · 2023Article
- Resistin-like molecules: a marker, mediator and therapeutic target for multiple diseases.Cell communication and signaling : CCS · 2023Review
- CD11c identifies microbiota and EGR2-dependent MHCIIEuropean journal of immunology · 2022Article
- Quantitative In-Depth Transcriptome Analysis Implicates Peritoneal Macrophages as Important Players in the Complement and Coagulation Systems.International journal of molecular sciences · 2022Article
- Dynamics of Host Immune Response Development DuringFrontiers in immunology · 2022Article
- Trickle infection withFrontiers in immunology · 2022Article
- Sex-Specific Modulation of the Host Transcriptome in the Spleen ofFrontiers in cellular and infection microbiology · 2022Article
- LKB1 deficiency upregulates RELM-α to drive airway goblet cell metaplasia.Cellular and molecular life sciences : CMLS · 2021Article
89 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Retnla (Resistin-like molecule alpha/FIZZ1) is induced during Th2 cytokine immune responses. However, the role of Retnla in Th2-type immunity is unknown. Here, using Retnla(-/-) mice and three distinct helminth models, we show that Retnla functions as a negative regulator of Th2 responses. Pulmonary granuloma formation induced by the eggs of the helminth parasite Schistosoma mansoni is dependent on IL-4 and IL-13 and associated with marked increases in Retnla expression. We found that both primary and secondary pulmonary granuloma formation were exacerbated in the absence of Retlna. The number of granuloma-associated eosinophils and serum IgE titers were also enhanced. Moreover, when chronically infected with S. mansoni cercariae, Retnla(-/-) mice displayed significant increases in granulomatous inflammation in the liver and the development of fibrosis and progression to hepatosplenic disease was markedly augmented. Finally, Retnla(-/-) mice infected with the gastrointestinal (GI) parasite Nippostrongylus brasiliensis had intensified lung pathology to migrating larvae, reduced fecundity, and accelerated expulsion of adult worms from the intestine, suggesting Th2 immunity was enhanced. When their immune responses were compared, helminth infected Retnla(-/-) mice developed stronger Th2 responses, which could be reversed by exogenous rRelmalpha treatment. Studies with several cytokine knockout mice showed that expression of Retnla was dependent on IL-4 and IL-13 and inhibited by IFN-gamma, while tissue localization and cell isolation experiments indicated that eosinophils and epithelial cells were the primary producers of Retnla in the liver and lung, respectively. Thus, the Th2-inducible gene Retnla suppresses resistance to GI nematode infection, pulmonary granulomatous inflammation, and fibrosis by negatively regulating Th2-dependent responses.
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