| Literature DB >> 17159982 |
Shinobu Saijo1, Noriyuki Fujikado, Takahisa Furuta, Soo-hyun Chung, Hayato Kotaki, Keisuke Seki, Katsuko Sudo, Shizuo Akira, Yoshiyuki Adachi, Naohito Ohno, Takeshi Kinjo, Kiwamu Nakamura, Kazuyoshi Kawakami, Yoichiro Iwakura.
Abstract
Dectin-1 is a C-type lectin involved in the recognition of beta-glucans found in the cell walls of fungi. We generated dectin-1-deficient mice to determine the importance of dectin-1 in the defense against pathogenic fungi. In vitro, beta-glucan-induced cytokine production from wild-type dendritic cells and macrophages was abolished in cells homozygous for dectin-1 deficiency ('dectin-1-knockout' cells). In vivo, dectin-1-knockout mice were more susceptible than wild-type mice to pneumocystis infection, even though their cytokine production was normal. However, pneumocystis-infected dectin-1-knockout macrophages did show defective production of reactive oxygen species. In contrast to those results, wild-type and dectin-1-knockout mice were equally susceptible to candida infection. Thus, dectin-1 is required for immune responses to some fungal infections, as protective immunity to pneumocystis, but not to candida, required dectin-1 for the production of antifungal reactive oxygen species.Entities:
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Year: 2006 PMID: 17159982 DOI: 10.1038/ni1425
Source DB: PubMed Journal: Nat Immunol ISSN: 1529-2908 Impact factor: 25.606