ArticleInfection and immunity2009
The C-type lectin SIGNR1 binds Schistosoma mansoni antigens in vitro, but SIGNR1-deficient mice have normal responses during schistosome infection.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- C-type lectin receptor signaling in schistosomiasis.Frontiers in immunology · 2026Review
- Review
- Pattern recognition receptor signaling and innate immune responses to schistosome infection.Frontiers in cellular and infection microbiology · 2022Review
- The C-type Lectin Receptor-Driven, Th17 Cell-Mediated Severe Pathology in Schistosomiasis: Not All Immune Responses to Helminth Parasites Are Th2 Dominated.Frontiers in immunology · 2019Review
- Ts-Hsp70 induces protective immunity against Trichinella spiralis infection in mouse by activating dendritic cells through TLR2 and TLR4.PLoS neglected tropical diseases · 2018Article
- CD209a Synergizes with Dectin-2 and Mincle to Drive Severe Th17 Cell-Mediated Schistosome Egg-Induced Immunopathology.Cell reports · 2018Article
- Schistosome egg antigens, including the glycoprotein IPSE/alpha-1, trigger the development of regulatory B cells.PLoS pathogens · 2017Article
- Novel O-linked methylated glycan antigens decorate secreted immunodominant glycoproteins from the intestinal nematode Heligmosomoides polygyrus.International journal for parasitology · 2016Article
- Dendritic cell expression of the C-type lectin receptor CD209a: A novel innate parasite-sensing mechanism inducing Th17 cells that drive severe immunopathology in murine schistosome infection.Experimental parasitology · 2015Article
- Innate Defense against Fungal Pathogens.Cold Spring Harbor perspectives in medicine · 2014Review
- CD209a expression on dendritic cells is critical for the development of pathogenic Th17 cell responses in murine schistosomiasis.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- A new tool to quantify receptor recruitment to cell contact sites during host-pathogen interaction.PLoS computational biology · 2014Article
- Helminth-excreted/secreted products are recognized by multiple receptors on DCs to block the TLR response and bias Th2 polarization in a cRAF dependent pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Parasitic infections: a role for C-type lectins receptors.BioMed research international · 2013Review
- The schistosoma granuloma: friend or foe?Frontiers in immunology · 2013Article
- Allergen-specific pattern recognition receptor pathways.Current opinion in immunology · 2010Review
- Immune modulation by Schistosoma mansoni antigens in NOD mice: effects on both innate and adaptive immune systems.Journal of biomedicine & biotechnology · 2010Article
- Modulation of dendritic cell responses by parasites: a common strategy to survive.Journal of biomedicine & biotechnology · 2010Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The de novo immune response to infectious organisms arises from the innate recognition of pathogen-associated molecular patterns (PAMPs) by the host's pattern recognition receptors (PRRs). As the generation of type 2 cytokine responses by the human trematode parasite Schistosoma mansoni is glycan mediated, there is a particular potential role for a C-type lectin receptor (CLR) to mediate the innate recognition of schistosome PAMPs. One such CLR, dendritic cell-specific intracellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN; CD209), has been shown to recognize glycans expressed by S. mansoni eggs. We show that SIGNR1 (SIGN-related 1; CD209b), a murine homologue of DC-SIGN that is expressed on macrophages, also binds both schistosome-soluble egg antigens and worm antigens in vitro. The generation of schistosome egg-induced pulmonary egg granulomas was not altered in SIGNR1-deficient mice. Following S. mansoni infection, the SIGNR1-deficient mice had an unaltered phenotype with an intact immunological response and no difference in pathology. In this study we demonstrate that although SIGNR1 recognizes S. mansoni antigens in vitro, this CLR is redundant during infection. This study highlights the finding that although there was binding of SIGNR1 to immunogenic factors produced in the S. mansoni life cycle, this recognition does not translate to a functional in vivo role for the PRR during infection.
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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.