{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,24]],"date-time":"2026-01-24T18:24:12Z","timestamp":1769279052571,"version":"3.49.0"},"reference-count":65,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2013,9,1]],"date-time":"2013-09-01T00:00:00Z","timestamp":1377993600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2013,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The opportunistic pathogen\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Pneumocystis jirovecii<\/jats:named-content>\n            is a significant cause of disease in HIV-infected patients and others with immunosuppressive conditions.\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Pneumocystis<\/jats:named-content>\n            can also cause complications in treatment following antiretroviral therapy or reversal of immunosuppressive therapy, as the newly reconstituted immune system can develop a pathological inflammatory response to remaining antigens or a previously undetected infection. To target \u03b2-(1,3)-glucan, a structural component of the\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Pneumocystis<\/jats:named-content>\n            cell wall with immune-stimulating properties, we have developed immunoadhesins consisting of the carbohydrate binding domain of Dectin-1 fused to the Fc regions of the 4 subtypes of murine IgG (mIgG). These immunoadhesins bind \u03b2-glucan with high affinity, and precoating the surface of zymosan with Dectin-1:Fc can reduce cytokine production by macrophages in an\n            <jats:italic>in vitro<\/jats:italic>\n            stimulation assay. All Dectin-1:Fc variants showed specificity of binding to the asci of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Pneumocystis murina<\/jats:named-content>\n            , but effector activity of the fusion molecules varied depending on Fc subtype. Dectin-1:mIgG2a Fc was able to reduce the viability of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">P. murina<\/jats:named-content>\n            in culture through a complement-dependent mechanism, whereas previous studies have shown the mIgG1 Fc fusion to increase macrophage-dependent killing. In an\n            <jats:italic>in vivo<\/jats:italic>\n            challenge model, systemic expression of Dectin-1:mIgG1 Fc significantly reduced ascus burden in the lung. When administered postinfection in a model of immune reconstitution inflammatory syndrome (IRIS), both Dectin-1:mIgG1 and Dectin-1:mIgG2a Fc reduced hypoxemia despite minimal effects on fungal burden in the lung. Taken together, these data indicate that molecules targeting \u03b2-glucan may provide a mechanism for treatment of fungal infection and for modulation of the inflammatory response to\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Pneumocystis<\/jats:named-content>\n            and other pathogens.\n          <\/jats:p>","DOI":"10.1128\/iai.00136-13","type":"journal-article","created":{"date-parts":[[2013,7,9]],"date-time":"2013-07-09T00:37:28Z","timestamp":1373330248000},"page":"3451-3462","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":24,"title":["Dectin Immunoadhesins and Pneumocystis Pneumonia"],"prefix":"10.1128","volume":"81","author":[{"given":"David M.","family":"Ricks","sequence":"first","affiliation":[{"name":"Department of Genetics, Louisiana State University Health Sciences Center (LSUHSC), New Orleans, Louisiana, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kong","family":"Chen","sequence":"additional","affiliation":[{"name":"Richard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mingquan","family":"Zheng","sequence":"additional","affiliation":[{"name":"Richard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chad","family":"Steele","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jay K.","family":"Kolls","sequence":"additional","affiliation":[{"name":"Richard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.3201\/eid1010.030985"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1378\/chest.08-2859"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1258\/ijsa.2012.011203"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1378\/chest.118.3.704"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-3062.2012.00739.x"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199001183220304"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1164\/ajrccm.155.1.9001290"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI114621"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.172.3.937"},{"key":"e_1_3_2_11_2","first-page":"1173","article-title":"Spontaneous Pneumocystis carinii pneumonia in immunodeficient mutant scid mice. 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