ArticleInfection and immunity2009
Complement receptor 3 deficiency influences lesion progression during Leishmania major infection in BALB/c mice.
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 20 papers.
What it found
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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.
The trial behind it
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- An overview of host immune responses against Leishmania spp. infections.Human molecular genetics · 2025Review
- Article
- Major Molecular Factors Related toFrontiers in immunology · 2022Review
- Complement receptor 3 mediates ruffle-like, actin-rich aggregates during phagocytosis of Leishmania infantum metacyclics.Experimental parasitology · 2021Article
- The Glycosylphosphatidylinositol Anchor: A Linchpin for Cell Surface Versatility of Trypanosomatids.Frontiers in cell and developmental biology · 2021Review
- β2 Integrin-Mediated Susceptibility toFrontiers in cellular and infection microbiology · 2021Article
- Macrophages as host, effector and immunoregulatory cells in leishmaniasis: Impact of tissue micro-environment and metabolism.Cytokine: X · 2020Article
- β2 Integrins-Multi-Functional Leukocyte Receptors in Health and Disease.International journal of molecular sciences · 2020Review
- Complement Receptor 3-Mediated Inhibition of Inflammasome Priming by Ras GTPase-Activating Protein DuringFrontiers in immunology · 2018Article
- The circadian clock in immune cells controls the magnitude of Leishmania parasite infection.Scientific reports · 2017Article
- The Src kinases Hck, Fgr and Lyn activate Arg to facilitate IgG-mediated phagocytosis and Leishmania infection.Journal of cell science · 2016Article
- Innate immunity against Leishmania infections.Cellular microbiology · 2015Review
- Ecotin-like ISP of L. major promastigotes fine-tunes macrophage phagocytosis by limiting the pericellular release of bradykinin from surface-bound kininogens: a survival strategy based on the silencing of proinflammatory G-protein coupled kinin B2 and B1 receptors.Mediators of inflammation · 2014Article
- Leishmania major inhibits IL-12 in macrophages by signalling through CR3 (CD11b/CD18) and down-regulation of ETS-mediated transcription.Parasite immunology · 2013Article
- Mechanisms of immune evasion in leishmaniasis.Advances in applied microbiology · 2013Article
- The Role of Vitamin D and Vitamin D Receptor in Immunity to Leishmania major Infection.Journal of parasitology research · 2012Article
- A mathematical model of CR3/TLR2 crosstalk in the context of Francisella tularensis infection.PLoS computational biology · 2012Article
- Innate immune activation and subversion of Mammalian functions by leishmania lipophosphoglycan.Journal of parasitology research · 2012Article
- Article
- Suppression of LPS-induced inflammatory responses in macrophages infected with Leishmania.Journal of inflammation (London, England) · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Leishmania major is an obligately intracellular protozoan parasite that causes cutaneous leishmaniasis. Like numerous intracellular pathogens, Leishmania exploits cell surface receptors as a means of entry into host cells. Complement receptor 3 (CR3; also called CD11b/CD18), a beta(2) integrin on phagocytic cells, is one such receptor. Ligation of CR3 has been shown to inhibit the production of interleukin-12, the cytokine that is pivotal in establishing the cell-mediated response necessary to combat intracellular infection. Here we investigate the role that CR3 plays in the establishment and progression of cutaneous leishmaniaisis in vivo. Dermal lesions of wild-type BALB/c mice are characteristically progressive and lead to extensive tissue necrosis coupled with elevated parasite burdens; CD11b-deficient BALB/c mice, however, demonstrate an intermediate phenotype characterized by chronic lesions and a reduced incidence of tissue damage. Infection followed by a reinfection challenge indicates that both susceptible (BALB/c) and resistant (C57BL/6) mice, regardless of CD11b status, develop resistance to L. major. In addition, CD11b does not bias the T helper cytokine response to L. major infection. Our results further indicate that CD11b is not necessary for disease resolution in resistant mice; rather, this protein appears to play a minor role in susceptibility.
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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.