ArticleScientific reports2021
Deficiency of lung-specific claudin-18 leads to aggravated infection with Cryptococcus deneoformans through dysregulation of the microenvironment in lungs.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- CLDN18.2-Targeted Therapy in Gastrointestinal Cancers.Cancers · 2025Review
- Functional landscape of mechanistic diversity in 27 claudin family members at tight junctions.Science advances · 2025Article
- Targeting Claudin18.2 for cancer theranostics: From molecular imaging to precision therapy.iScience · 2025Review
- Correlation of CLDN18.2 and Tumor Microenvironment in Gastric Cancer: A Systematic Review.Cancers · 2025Review
- Claudins in Cancer: A Current and Future Therapeutic Target.International journal of molecular sciences · 2024Review
- Expression patterns of claudins in cancer.Heliyon · 2023Review
- Tetrahydrocurcumin (THC) enhanced the clearance of Cryptococcus deneoformans during infection in vivo.Antonie van Leeuwenhoek · 2023Article
- Glucuronoxylomannan intranasal challenge prior to Cryptococcus neoformans pulmonary infection enhances cerebral cryptococcosis in rodents.PLoS pathogens · 2023Article
- Mouse Model of Latent Cryptococcal Infection and Reactivation.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Targeting CLDN18.2 in cancers of the gastrointestinal tract: New drugs and new indications.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
22 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cryptococcus deneoformans is an opportunistic fungal pathogen that infects the lungs via airborne transmission and frequently causes fatal meningoencephalitis. Claudins (Cldns), a family of proteins with 27 members found in mammals, form the tight junctions within epithelial cell sheets. Cldn-4 and 18 are highly expressed in airway tissues, yet the roles of these claudins in respiratory infections have not been clarified. In the present study, we analyzed the roles of Cldn-4 and lung-specific Cldn-18 (luCldn-18) in host defense against C. deneoformans infection. luCldn-18-deficient mice exhibited increased susceptibility to pulmonary infection, while Cldn-4-deficient mice had normal fungal clearance. In luCldn-18-deficient mice, production of cytokines including IFN-γ was significantly decreased compared to wild-type mice, although infiltration of inflammatory cells including CD4
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Registered trials
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