{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T21:09:03Z","timestamp":1793048943245,"version":"4.5.0"},"reference-count":35,"publisher":"National Academy of Sciences","issue":"4","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2007,1,23]]},"abstract":"<jats:p>\n                    Successful infection by fungal pathogens depends on subversion of host immune mechanisms that detect conserved cell wall components such as \u03b2-glucans. A less common polysaccharide, \u03b1-(1,3)-glucan, is a cell wall constituent of most fungal respiratory pathogens and has been correlated with pathogenicity or linked directly to virulence. However, the precise mechanism by which \u03b1-(1,3)-glucan promotes fungal virulence is unknown. Here, we show that \u03b1-(1,3)-glucan is present in the outermost layer of the\n                    <jats:italic>Histoplasma capsulatum<\/jats:italic>\n                    yeast cell wall and contributes to pathogenesis by concealing immunostimulatory \u03b2-glucans from detection by host phagocytic cells. Production of proinflammatory TNF\u03b1 by phagocytes was suppressed either by the presence of the \u03b1-(1,3)-glucan layer on yeast cells or by RNA interference based depletion of the host \u03b2-glucan receptor\n                    <jats:italic>dectin-1<\/jats:italic>\n                    . Thus, we have functionally defined key molecular components influencing the initial host\u2013pathogen interaction in histoplasmosis and have revealed an important mechanism by which\n                    <jats:italic>H. capsulatum<\/jats:italic>\n                    thwarts the host immune system. Furthermore, we propose that the degree of this evasion contributes to the difference in pathogenic potential between dimorphic fungal pathogens and opportunistic fungi.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0609848104","type":"journal-article","created":{"date-parts":[[2007,1,16]],"date-time":"2007-01-16T22:18:23Z","timestamp":1168985903000},"page":"1366-1370","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":392,"title":["<i>Histoplasma capsulatum<\/i>\n                    \u03b1-(1,3)-glucan blocks innate immune recognition by the \u03b2-glucan receptor"],"prefix":"10.1073","volume":"104","author":[{"given":"Chad A.","family":"Rappleye","sequence":"first","affiliation":[{"name":"Department of Molecular Microbiology, Washington University, St. Louis, MO 63110"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda Groppe","family":"Eissenberg","sequence":"additional","affiliation":[{"name":"Department 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