{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T04:44:43Z","timestamp":1770698683694,"version":"3.49.0"},"reference-count":60,"publisher":"Rockefeller University Press","issue":"8","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1998,4,20]]},"abstract":"<jats:p>The induction of type 1 immune responses (interleukin [IL]-12, interferon [IFN]-\u03b3) has been shown to be important in mediating protection against many intracellular infections including Histoplasma capsulatum. Costimulatory molecules such as CD40 ligand (CD40L) have been shown to be a central regulator of type 1 responses in vivo. To study the role of CD40L in mediating protection against infection with H. capsulatum, CD40L-deficient (CD40L\u2212\/\u2212) and CD40L+\/+ mice were infected with H. capsulatum and assessed for various parameters. After a lethal challenge of H. capsulatum, CD40L\u2212\/\u2212 mice were not substantially different from CD40L+\/+ mice in terms of mortality, fungal burden, or production of IFN-\u03b3, IL-12, nitric oxide, or tumor necrosis factor \u03b1. Moreover, CD40L\u2212\/\u2212 mice treated with anti\u2013IFN-\u03b3 or anti\u2013IL-12 at the time of infection had accelerated mortality, providing further evidence that IL-12 and IFN-\u03b3 are produced in vivo in the absence of CD40L. In addition, CD40L\u2212\/\u2212 mice infected with a sublethal dose of H. capsulatum survived infection, whereas all mice infected with the same dose and treated with anti\u2013IFN-\u03b3 had accelerated mortality, demonstrating that IFN-\u03b3 but not CD40L was essential for primary immunity to H. capsulatum infection. Interestingly, depletion of either CD4+ or CD8+ T cells resulted in accelerated mortality in CD40L\u2212\/\u2212 mice, suggesting a critical role for these cells in response to infection. Finally, CD40L\u2212\/\u2212 mice initially infected with a sublethal dose of H. capsulatum were protected from secondary infection with a lethal dose of H. capsulatum, demonstrating that CD40L is not required for the maintenance of memory immunity.<\/jats:p>","DOI":"10.1084\/jem.187.8.1315","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:49:30Z","timestamp":1027702170000},"page":"1315-1324","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":38,"title":["CD40 Ligand Is Not Essential for Induction of Type 1 Cytokine Responses or Protective Immunity after Primary or Secondary Infection With <i>Histoplasma capsulatum <\/i>"],"prefix":"10.1084","volume":"187","author":[{"given":"Ping","family":"Zhou","sequence":"first","affiliation":[{"name":"From the Clinical Immunology Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National 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