ArticleNature communications2019
A small secreted protein triggers a TLR2/4-dependent inflammatory response during invasive Candida albicans infection.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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
43 citing papers in PubMed.
- The Candida albicans exotoxin candidalysin promotes alcohol-associated liver disease.Journal of hepatology · 2020Trial
- Antifungal effect ofIranian journal of microbiology · 2026Article
- Bacteria-mimicking cancer cells reprogram macrophages via multiple pattern recognition receptor pathways for cancer immunotherapy.Signal transduction and targeted therapy · 2026Article
- The role of L-type amino acid transporter 1 in the pathogenicity ofMicrobiology spectrum · 2026Article
- Fungal extracellular vesicles mediate conserved cross-species communication and immunomodulation.mBio · 2026Article
- p24 family proteins are critical for cell wall integrity, protein secretion, and virulence inmSphere · 2026Article
- Dual Disruption of the Immune Cytokine Spätzle Facilitates Fungal Infection of Diverse Insect Hosts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Innate airway immune response to fungal allergens.Frontiers in immunology · 2026Review
- The pathogenicity and future treatment strategies ofFrontiers in cellular and infection microbiology · 2026Review
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- Breaking the durability barrier with d band optimized Cu Fe twin crystal nanozymes for long term suppression of Botrytis cinerea.Nature communications · 2025Article
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- Enhancement of melanoma aggressiveness via p38-MAPK, HIF-1α pathways, and metabolic reprogramming induced by Candida albicans.Scientific reports · 2025Article
- Article
- Fungal Als proteins hijack host death effector domains to promote inflammasome signaling.Nature communications · 2025Article
- Invasive fungal infections in patients with liver disease: immunological and clinical considerations for the intensive care unit.Intensive care medicine · 2025Review
- Schizophrenia-associated alterations in fecal mycobiota and systemic immune dysfunction: a cohort study of elderly Chinese patients.Frontiers in immunology · 2025Article
- Cinnamaldehyde triggers cell wall remodeling and enhances macrophage-mediated phagocytic clearance ofFrontiers in cellular and infection microbiology · 2025Article
- Bioinformatics-Driven mRNA-Based Vaccine Design for Controlling Tinea Cruris Induced byPharmaceutics · 2024Article
- Innate immune signal transduction pathways to fungal infection: Components and regulation.Cell insight · 2024Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Candida albicans can switch from commensal to pathogenic mode, causing mucosal or disseminated candidiasis. The host relies on pattern-recognition receptors including Toll-like receptors (TLRs) and C-type lectin receptors (CLRs) to sense invading fungal pathogens and launch immune defense mechanisms. However, the complex interplay between fungus and host innate immunity remains incompletely understood. Here we report that C. albicans upregulates expression of a small secreted cysteine-rich protein Sel1 upon encountering limited nitrogen and abundant serum. Sel1 activates NF-κB and MAPK signaling pathways, leading to expression of proinflammatory cytokines and chemokines. Comprehensive genetic and biochemical analyses reveal both TLR2 and TLR4 are required for the recognition of Sel1. Further, SEL1-deficient C. albicans display an impaired immune response in vivo, causing increased morbidity and mortality in a bloodstream infection model. We identify a critical component in the Candida-host interaction that opens a new avenue to tackle Candida infection and inflammation.
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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.