ArticleInfection and immunity2015
Dectin-2 deficiency promotes Th2 response and mucin production in the lungs after pulmonary infection with Cryptococcus neoformans.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 66 citations in OpenAlex.
- Review
- Cryptococcal infection: host immunity, immune evasion and emerging immunotherapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
- Card9 Broadly Regulates Host Immunity against Experimental PulmonaryJournal of fungi (Basel, Switzerland) · 2024Article
- Inbred Mouse Models inJournal of fungi (Basel, Switzerland) · 2024Review
- Innate phase production of IFN-γ by memory and effector T cells expressing early activation marker CD69 during infection withInfection and immunity · 2024Article
- Dendritic Cells: Multifunctional Roles in Host Defenses toJournal of fungi (Basel, Switzerland) · 2023Review
- CD146 deficiency promotes inflammatory type 2 responses in pulmonary cryptococcosis.Medical microbiology and immunology · 2023Article
- Innate Pulmonary Phagocytes and Their Interactions with PathogenicJournal of fungi (Basel, Switzerland) · 2023Review
- Mouse Model of Latent Cryptococcal Infection and Reactivation.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Inhibition of myeloid-derived suppressor cell arginase-1 production enhances T-cell-based immunotherapy against Cryptococcus neoformans infection.Nature communications · 2022Article
- Review
- 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
- 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
- Pneumocystis carinii Major Surface Glycoprotein Dampens Macrophage Inflammatory Responses to Fungal β-Glucan.The Journal of infectious diseases · 2020Article
- Review
- T Cell Antifungal Immunity and the Role of C-Type Lectin Receptors.Trends in immunology · 2020Review
- It takes a village: Phagocytes play a central role in fungal immunity.Seminars in cell & developmental biology · 2019Review
- Cryptococcus gattii alters immunostimulatory potential in response to the environment.PloS one · 2019Article
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dectin-2 is a C-type lectin receptor that recognizes high mannose polysaccharides. Cryptococcus neoformans, a yeast-form fungal pathogen, is rich in polysaccharides in its cell wall and capsule. In the present study, we analyzed the role of Dectin-2 in the host defense against C. neoformans infection. In Dectin-2 gene-disrupted (knockout) (Dectin-2KO) mice, the clearance of this fungus and the inflammatory response, as shown by histological analysis and accumulation of leukocytes in infected lungs, were comparable to those in wild-type (WT) mice. The production of type 2 helper T (Th2) cytokines in lungs was higher in Dectin-2KO mice than in WT mice after infection, whereas there was no difference in the levels of production of Th1, Th17, and proinflammatory cytokines between these mice. Mucin production was significantly increased in Dectin-2KO mice, and this increase was reversed by administration of anti-interleukin 4 (IL-4) monoclonal antibody (MAb). The levels of expression of β1-defensin, cathelicidin, surfactant protein A (Sp-A), and Sp-D in infected lungs were comparable between these mice. In in vitro experiments, IL-12p40 and tumor necrosis factor alpha (TNF-α) production and expression of CD86 and major histocompatibility complex (MHC) class II by bone marrow-derived dendritic cells and alveolar macrophages were completely abrogated in Dectin-2KO mice. Finally, the disrupted lysates of C. neoformans, but not of whole yeast cells, activated Dectin-2-triggered signaling in an assay with nuclear factor of activated T cells (NFAT)-green fluorescent protein (GFP) reporter cells expressing this receptor. These results suggest that Dectin-2 may oppose the Th2 response and IL-4-dependent mucin production in the lungs after infection with C. neoformans, and it may not be required for the production of Th1, Th17, and proinflammatory cytokines or for clearance of this fungal pathogen.
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