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Nature Immunology 8, 39–46 (1 January 2007) | doi:10.1038/ni1425

Dectin-1 is required for host defense against Pneumocystis carinii but not against Candida albicans

Shinobu Saijo , 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

Dectin-1 is a C-type lectin involved in the recognition of β-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, β-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.