ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Integrin αXβ₂ is a leukocyte receptor for Candida albicans and is essential for protection against fungal infections.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 32 citations in OpenAlex.
- Integrin ß4 is a receptor for emerging fungal pathogens from the genera Lomentospora and Scedosporium.PLoS pathogens · 2026Article
- Hyphal Als proteins act as CR3 ligands to promote immune responses against Candida albicans.Nature communications · 2024Article
- A New Phenotype inmBio · 2023Article
- COVID-19-associated fungal infections.Nature microbiology · 2022Review
- How Gut Bacterial Dysbiosis Can PromoteMicroorganisms · 2022Review
- H89 Treatment Reduces Intestinal Inflammation andMicroorganisms · 2020Article
- How Fungal Glycans Modulate Platelet Activation via Toll-Like Receptors Contributing to the Escape ofAntibiotics (Basel, Switzerland) · 2020Review
- Role of β2 Integrins in Neutrophils and Sepsis.Infection and immunity · 2020Review
- Article
- Organ-specific mechanisms linking innate and adaptive antifungal immunity.Seminars in cell & developmental biology · 2019Review
- Liver macrophages in tissue homeostasis and disease.Nature reviews. Immunology · 2017Review
- Distinct Effects of Integrins αXβ2 and αMβ2 on Leukocyte Subpopulations during Inflammation and Antimicrobial Responses.Infection and immunity · 2017Article
- Article
- Thriving within the host: Candida spp. interactions with phagocytic cells.Medical microbiology and immunology · 2013Review
- Binding of Soluble Yeast β-Glucan to Human Neutrophils and Monocytes is Complement-Dependent.Frontiers in immunology · 2013Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The opportunistic fungus Candida albicans is one of the leading causes of infections in immunocompromised patients, and innate immunity provides a principal mechanism for protection from the pathogen. In the present work, the role of integrin α(X)β₂ in the pathogenesis of fungal infection was assessed. Both purified α(X)β₂ and α(X)β₂-expressing human epithelial kidney 293 cells recognized and bound to the fungal hyphae of SC5314 strain of C. albicans but not to the yeast form or to hyphae of a strain deficient in the fungal mannoprotein, Pra1. The binding of the integrin to the fungus was inhibited by β-glucans but not by mannans, implicating a lectin-like activity in recognition but distinct in specificity from that of α(M)β₂. Mice deficient in α(X)β₂ were more prone to systemic infection with the LD₅₀ fungal inoculum decreasing 3-fold in α(X)β₂-deficient mice compared with wild-type mice. After challenging i.v. with 1.5 × 10⁴ cell/g, 60% of control C57BL/6 mice died within 14 d compared with 100% mortality of α(X)β₂-deficient mice within 9 d. Organs taken from α(X)β₂-deficient mice 16 h postinfection revealed a 10-fold increase in fungal invasion into the brain and a 2-fold increase into the liver. These data indicate that α(X)β₂ is important for protection against systemic C. albicans infections and macrophage subsets in the liver, Kupffer cells, and in the brain, microglial cells use α(X)β₂ to control fungal invasion.
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