{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T17:05:18Z","timestamp":1761843918170},"reference-count":79,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2010,1,1]],"date-time":"2010-01-01T00:00:00Z","timestamp":1262304000000},"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":[[2010,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Cryptococcus neoformans<\/jats:italic>causes severe, and often fatal, disease (cryptococcosis) in immunocompromised patients, particularly in those with HIV\/AIDS. Although resistance to cryptococcosis requires intact T-cell immunity, a possible role for antibody\/B cells in protection against natural disease has not been definitively established. Previous studies of the antibody response to the<jats:italic>C. neoformans<\/jats:italic>capsular polysaccharide glucuronoxylomannan (GXM) have demonstrated that patients who are at increased risk for cryptococcosis have lower serum levels of GXM-reactive IgM than those who are not at risk, leading to the hypothesis that IgM might contribute to resistance to cryptococcosis. To determine the influence of IgM on susceptibility to systemic cryptococcosis in a murine model, we compared the survival of mice deficient in serum IgM (secretory IgM deficient [sIgM<jats:sup>\u2212\/\u2212<\/jats:sup>]) and C57BL\/6 \u00d7 129Sv (control) mice after intraperitoneal infection with<jats:italic>C. neoformans<\/jats:italic>strain 24067 and analyzed the splenic B- and T-cell subsets by flow cytometry and the serum and splenic cytokine\/chemokine and serum antibody profiles of each mouse strain. The results showed that sIgM<jats:sup>\u2212\/\u2212<\/jats:sup>mice survived significantly longer than control mice when challenged with 10<jats:sup>5<\/jats:sup>CFU of<jats:italic>C. neoformans<\/jats:italic>24067. Nai\u0308ve sIgM<jats:sup>\u2212\/\u2212<\/jats:sup>mice had higher levels of B-1 (CD5<jats:sup>+<\/jats:sup>) B cells, proinflammatory mediators (interleukin-6 [IL-6], IL-1\u03b2, MIP-1\u03b2, tumor necrosis factor alpha [TNF-\u03b1], and gamma interferon [IFN-\u03b3]), and anti-inflammatory mediators (IL-10 and IL-13) and significantly higher titers of GXM-specific IgG2a 3 weeks postinfection. In addition, CD5<jats:sup>+<\/jats:sup>splenocytes from both mouse strains had fungicidal activity against<jats:italic>C. neoformans<\/jats:italic>. Taken together, these results suggest that the inflammatory milieu in sIgM<jats:sup>\u2212\/\u2212<\/jats:sup>mice might confer enhanced resistance to systemic cryptococcosis, stemming in part from the antifungal activity of B-1 B cells.<\/jats:p>","DOI":"10.1128\/iai.00506-09","type":"journal-article","created":{"date-parts":[[2009,11,10]],"date-time":"2009-11-10T02:44:45Z","timestamp":1257821085000},"page":"441-452","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":15,"title":["Improved Survival of Mice Deficient in Secretory Immunoglobulin M following Systemic Infection with<i>Cryptococcus neoformans<\/i>"],"prefix":"10.1128","volume":"78","author":[{"given":"Krishanthi S.","family":"Subramaniam","sequence":"first","affiliation":[{"name":"Department of Microbiology &amp; Immunology"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kausik","family":"Datta","sequence":"additional","affiliation":[{"name":"Department of Microbiology &amp; Immunology"},{"name":"Johns Hopkins University School of Medicine, Baltimore, Maryland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthew S.","family":"Marks","sequence":"additional","affiliation":[{"name":"Department of Medicine, Albert Einstein College of Medicine, Bronx, New York"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Liise-anne","family":"Pirofski","sequence":"additional","affiliation":[{"name":"Department of Microbiology &amp; Immunology"},{"name":"Department of Medicine, Albert Einstein College of Medicine, Bronx, New York"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cytogfr.2007.01.007"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.63.5.1725-1731.1995"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.65.2.525-530.1997"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/13.9.1193"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.170.7.3819"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V99.2.427"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.192.2.271"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.69.10.6445-6455.2001"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1097\/QAI.0b013e3181a56f2e"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1093\/intimm\/10.8.1185"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.63.4.1218-1222.1995"},{"key":"e_1_3_2_13_2","doi-asserted-by":"crossref","first-page":"4776","DOI":"10.4049\/jimmunol.160.10.4776","volume":"160","year":"1998","unstructured":"Boes, M., C. 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