ArticleInfection and immunity2014
Defect of CARD9 leads to impaired accumulation of gamma interferon-producing memory phenotype T cells in lungs and increased susceptibility to pulmonary infection with Cryptococcus neoformans.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 60 citations in OpenAlex.
- Review
- Unraveling CARD9 Mutations in Deep Dermatophytosis: A Genetic Gateway to Fungal Invasion and Immune Dysfunction.Journal of fungi (Basel, Switzerland) · 2026Review
- Immunological mechanism behind reactivated cryptococcosis in persistently infected mice following FTY720 treatment.Infection and immunity · 2026Article
- Systemic administration of liposomal trehalose dimycolate induces NK1.1⁺ cell mediated antitumor immunity in bladder cancer.BMC cancer · 2026Article
- Intracranial infections ofFrontiers in immunology · 2025Review
- State of the Field: Cytotoxic Immune Cell Responses inJournal of fungi (Basel, Switzerland) · 2024Review
- Card9 Broadly Regulates Host Immunity against Experimental PulmonaryJournal of fungi (Basel, Switzerland) · 2024Article
- Innate phase production of IFN-γ by memory and effector T cells expressing early activation marker CD69 during infection withInfection and immunity · 2024Article
- The CARD9 Gene in Koalas (Journal of fungi (Basel, Switzerland) · 2024Article
- Role of CARD9 in Cell- and Organ-Specific Immune Responses in Various Infections.International journal of molecular sciences · 2024Review
- Mouse Model of Latent Cryptococcal Infection and Reactivation.Methods in molecular biology (Clifton, N.J.) · 2023Article
- CARD9 in host immunity to fungal, bacterial, viral, and parasitic infections: An update.Frontiers in microbiology · 2022Review
- Deficiency of lung-specific claudin-18 leads to aggravated infection with Cryptococcus deneoformans through dysregulation of the microenvironment in lungs.Scientific reports · 2021Article
- Role of Dectin-2 in the Phagocytosis of Cryptococcus neoformans by Dendritic Cells.Infection and immunity · 2021Article
- Gut microbiota and inflammatory bowel disease: The current status and perspectives.World journal of clinical cases · 2021Review
- Limited Role of Mincle in the Host Defense against Infection with Cryptococcus deneoformans.Infection and immunity · 2020Article
- A critical role for CARD9 in pneumocystis pneumonia host defence.Cellular microbiology · 2020Article
- During Aspergillus Infection, Monocyte-Derived DCs, Neutrophils, and Plasmacytoid DCs Enhance Innate Immune Defense through CXCR3-Dependent Crosstalk.Cell host & microbe · 2020Article
- Review
- Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caspase recruitment domain-containing protein 9 (CARD9) is an adaptor molecule signal that is critical for NF-κB activation and is triggered through C-type lectin receptors (CLRs), which are pattern recognition receptors that recognize carbohydrate structures. Previous studies have reported that Cryptococcus neoformans, a fungal pathogen that causes meningoencephalitis in AIDS patients, is recognized through some CLRs, such as mannose receptors or DC-SIGN. However, the role of CARD9 in the host defense against cryptococcal infection remains to be elucidated. In the present study, we analyzed the role of CARD9 in the host defense against pulmonary infection with C. neoformans. CARD9 gene-disrupted (knockout [KO]) mice were highly susceptible to this infection, as shown by the reduced fungal clearance in the infected lungs of CARD9 KO mice, compared to that in wild-type (WT) mice. Gamma interferon (IFN-γ) production was strongly reduced in CARD9 KO mice during the innate-immunity phase of infection. Reduced IFN-γ synthesis was due to impaired accumulation of NK and memory phenotype T cells, which are major sources of IFN-γ innate-immunity-phase production; a reduction in the accumulation of these cells was correlated with reduced CCL4, CCL5, CXCL9, and CXCL10 synthesis. However, differentiation of Th17 cells, but not of Th1 cells, was impaired at the adaptive-immunity phase in CARD9 KO mice compared to WT mice, although there was no significant difference in the infection susceptibility between interleukin 17A (IL-17A) KO and WT mice. These results suggest that CARD9 KO mice are susceptible to C. neoformans infection probably due to the reduced accumulation of IFN-γ-expressing NK and memory phenotype T cells at the early stage of infection.
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