{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T21:17:11Z","timestamp":1790371031491,"version":"4.1.0"},"reference-count":66,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2018,2,1]],"date-time":"2018-02-01T00:00:00Z","timestamp":1517443200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Pneumocystis is an important fungal pathogen that causes life-threatening pneumonia in patients with AIDS and malignancy. Lung fungal pathogens are recognized by C-type lectin receptors (CLRs), which bind specific ligands and stimulate innate immune responses. The CLR Dectin-1 was previously shown to mediate immune responses to Pneumocystis spp. For this reason, we investigated a potential role for Dectin-2. Rats with Pneumocystis pneumonia (PCP) exhibited elevated Dectin-2 mRNA levels. Soluble Dectin-2 carbohydrate-recognition domain fusion protein showed binding to intact Pneumocystis carinii (Pc) and to native Pneumocystis major surface glycoprotein\/glycoprotein A (Msg\/gpA). RAW macrophage cells expressing V5-tagged Dectin-2 displayed enhanced binding to Pc and increased protein tyrosine phosphorylation. Furthermore, the binding of Pc to Dectin-2 resulted in Fc receptor-\u03b3\u2013mediated intracellular signaling. Alveolar macrophages from Dectin-2\u2013deficient mice (Dectin-2\u2212\/\u2212) showed significant decreases in phospho-Syk activation after challenge with Pc cell wall components. Stimulation of Dectin-2\u2212\/\u2212 alveolar macrophages with Pc components showed significant decreases in the proinflammatory cytokines IL-6 and TNF-\u03b1. Finally, during infection with Pneumocystis murina, Dectin-2\u2212\/\u2212 mice displayed downregulated mRNA expression profiles of other CLRs implicated in fungal immunity. Although Dectin-2\u2212\/\u2212 alveolar macrophages had reduced proinflammatory cytokine release in vitro, Dectin-2\u2212\/\u2212 deficiency did not reduce the overall resistance of these mice in the PCP model, and organism burdens were statistically similar in the long-term immunocompromised and short-term immunocompetent PCP models. These results suggest that Dectin-2 participates in the initial innate immune signaling response to Pneumocystis, but its deficiency does not impair resistance to the organism.<\/jats:p>","DOI":"10.1165\/rcmb.2016-0335oc","type":"journal-article","created":{"date-parts":[[2017,9,8]],"date-time":"2017-09-08T17:11:19Z","timestamp":1504890679000},"page":"232-240","source":"Crossref","is-referenced-by-count":38,"title":["Dectin-2 Is a C-Type Lectin Receptor that Recognizes\n                    <i>Pneumocystis<\/i>\n                    and Participates in Innate Immune Responses"],"prefix":"10.1093","volume":"58","author":[{"given":"Theodore J.","family":"Kottom","sequence":"first","affiliation":[{"name":"Thoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deanne M.","family":"Hebrink","sequence":"additional","affiliation":[{"name":"Thoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paige E.","family":"Jenson","sequence":"additional","affiliation":[{"name":"Thoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paige L.","family":"Marsolek","sequence":"additional","affiliation":[{"name":"Thoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcel","family":"W\u00fcthrich","sequence":"additional","affiliation":[{"name":"Department of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huafeng","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce","family":"Klein","sequence":"additional","affiliation":[{"name":"Department of Pediatrics"},{"name":"Department of Internal Medicine, and"},{"name":"Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, University of Wisconsin Hospital and Clinics, Madison, Wisconsin; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sho","family":"Yamasaki","sequence":"additional","affiliation":[{"name":"Division of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew H.","family":"Limper","sequence":"additional","affiliation":[{"name":"Thoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2018,2,1]]},"reference":[{"key":"2026012222031423500_bib1","doi-asserted-by":"crossref","first-page":"165rv13","DOI":"10.1126\/scitranslmed.3004404","article-title":"Hidden killers: human fungal infections","volume":"4","author":"Brown","year":"2012","journal-title":"Sci Transl Med"},{"key":"2026012222031423500_bib2","doi-asserted-by":"crossref","first-page":"996","DOI":"10.1080\/15572536.2006.11832628","article-title":"Early diverging Ascomycota: phylogenetic divergence and related evolutionary enigmas","volume":"98","author":"Sugiyama","year":"2006","journal-title":"Mycologia"},{"key":"2026012222031423500_bib3","doi-asserted-by":"crossref","first-page":"fov046","DOI":"10.1093\/femsyr\/fov046","article-title":"Pathobiology of Pneumocystis pneumonia: life cycle, cell wall and cell signal transduction","volume":"15","author":"Skalski","year":"2015","journal-title":"FEMS Yeast Res"},{"key":"2026012222031423500_bib4","doi-asserted-by":"crossref","first-page":"2487","DOI":"10.1056\/NEJMra032588","article-title":"Pneumocystis pneumonia","volume":"350","author":"Thomas","year":"2004","journal-title":"N Engl J Med"},{"key":"2026012222031423500_bib5","doi-asserted-by":"crossref","first-page":"661","DOI":"10.1053\/rmed.2001.1119","article-title":"Independent risk of mechanical ventilation for AIDS-related Pneumocystis carinii pneumonia associated with bronchoalveolar lavage neutrophilia","volume":"95","author":"Bang","year":"2001","journal-title":"Respir Med"},{"key":"2026012222031423500_bib6","first-page":"1058","article-title":"Prognostic value of interleukin-8 in AIDS-associated Pneumocystis carinii pneumonia","volume":"151","author":"Benfield","year":"1995","journal-title":"Am J Respir Crit Care Med"},{"key":"2026012222031423500_bib7","doi-asserted-by":"crossref","first-page":"1204","DOI":"10.1164\/ajrccm\/140.5.1204","article-title":"Pneumocystis carinii pneumonia. 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