ArticleJournal of immunology (Baltimore, Md. : 1950)2014
The C5a anaphylatoxin receptor (C5aR1) protects against Listeria monocytogenes infection by inhibiting type 1 IFN expression.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Complement Anaphylatoxin C5a-Induced Mouse Lymphatic Functions Modulate Interactions Between Endothelial Cells and T Lymphocytes.Immune network · 2026Article
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Cell Death and Infection: Implications for Host and Microbe.Advances in experimental medicine and biology · 2025Review
- FBXO11 governs macrophage cell death and inflammation in response to bacterial toxins.Life science alliance · 2023Article
- C3aR plays both sides in regulating resistance to bacterial infections.PLoS pathogens · 2022Review
- Enrichment of type I interferon signaling in colonic group 2 innate lymphoid cells in experimental colitis.Frontiers in immunology · 2022Article
- Protective role of host complement system inFrontiers in immunology · 2022Article
- More than a Pore: Nonlytic Antimicrobial Functions of Complement and Bacterial Strategies for Evasion.Microbiology and molecular biology reviews : MMBR · 2021Review
- Role of the C5a-C5a receptor axis in the inflammatory responses of the lungs after experimental polytrauma and hemorrhagic shock.Scientific reports · 2021Article
- Single-cell transcriptome profiling of an adult human cell atlas of 15 major organs.Genome biology · 2020Article
- From Classical to Unconventional: The Immune Receptors Facilitating Platelet Responses to Infection and Inflammation.Biology · 2020Review
- Circadian Clock and Complement Immune System-Complementary Control of Physiology and Pathology?Frontiers in cellular and infection microbiology · 2020Review
- The Second Receptor for C5a, C5aR2, Is Detrimental to Mice during Systemic Infection withJournal of immunology (Baltimore, Md. : 1950) · 2019Article
- Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019Article
- The Complement Anaphylatoxins C5a and C3a Suppress IFN-β Production in Response toJournal of immunology (Baltimore, Md. : 1950) · 2017Article
- Innate and adaptive immunologic functions of complement in the host response to Listeria monocytogenes infection.Immunobiology · 2016Review
- Type I IFN Does Not Promote Susceptibility to Foodborne Listeria monocytogenes.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Listeria monocytogenes is a major cause of mortality resulting from food poisoning in the United States. In mice, C5 has been genetically linked to host resistance to listeriosis. Despite this genetic association, it remains poorly understood how C5 and its activation products, C5a and C5b, confer host protection to this Gram-positive intracellular bacterium. In this article, we show in a systemic infection model that the major receptor for C5a, C5aR1, is required for a normal robust host immune response against L. monocytogenes. In comparison with wild-type mice, C5aR1(-/-) mice had reduced survival and increased bacterial burden in their livers and spleens. Infected C5aR1(-/-) mice exhibited a dramatic reduction in all major subsets of splenocytes, which was associated with elevated caspase-3 activity and increased TUNEL staining. Because type 1 IFN has been reported to impede the host response to L. monocytogenes through the promotion of splenocyte death, we examined the effect of C5aR1 on type 1 IFN expression in vivo. Indeed, serum levels of IFN-α and IFN-β were significantly elevated in L. monocytogenes-infected C5aR1(-/-) mice. Similarly, the expression of TRAIL, a type 1 IFN target gene and a proapoptotic factor, was elevated in NK cells isolated from infected C5aR1(-/-) mice. Treatment of C5aR1(-/-) mice with a type 1 IFNR blocking Ab resulted in near-complete rescue of L. monocytogenes-induced mortality. Thus, these findings reveal a critical role for C5aR1 in host defense against L. monocytogenes through the suppression of type 1 IFN expression.
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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.