{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Leopold Wager CM"],"funding":["BLRD VA","NIAID NIH HHS"],"pagination":["4513-27"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4645398"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["83(12)"],"pubmed_abstract":["Cryptococcus neoformans, the predominant etiological agent of cryptococcosis, is an opportunistic fungal pathogen that primarily affects AIDS patients and patients undergoing immunosuppressive therapy. In immunocompromised individuals, C. neoformans can lead to life-threatening meningoencephalitis. Studies using a virulent strain of C. neoformans engineered to produce gamma interferon (IFN-γ), denoted H99γ, demonstrated that protection against pulmonary C. neoformans infection is associated with the generation of a T helper 1 (Th1)-type immune response and signal transducer and activator of transcription 1 (STAT1)-mediated classical (M1) macrophage activation. However, the critical mechanism by which M1 macrophages mediate their anti-C. neoformans activity remains unknown. The current stud"],"journal":["Infection and immunity"],"pubmed_title":["STAT1 signaling within macrophages is required for antifungal activity against Cryptococcus neoformans."],"pmcid":["PMC4645398"],"funding_grant_id":["R01 AI071752","R21 AI100893","R21AI100893","I01 BX000656","2R01AI071752"],"pubmed_authors":["Hole CR","Leopold Wager CM","Mueller M","Wozniak KL","Wormley FL","Olszewski MA"],"additional_accession":[]},"is_claimable":false,"name":"STAT1 signaling within macrophages is required for antifungal activity against Cryptococcus neoformans.","description":"Cryptococcus neoformans, the predominant etiological agent of cryptococcosis, is an opportunistic fungal pathogen that primarily affects AIDS patients and patients undergoing immunosuppressive therapy. In immunocompromised individuals, C. neoformans can lead to life-threatening meningoencephalitis. Studies using a virulent strain of C. neoformans engineered to produce gamma interferon (IFN-γ), denoted H99γ, demonstrated that protection against pulmonary C. neoformans infection is associated with the generation of a T helper 1 (Th1)-type immune response and signal transducer and activator of transcription 1 (STAT1)-mediated classical (M1) macrophage activation. However, the critical mechanism by which M1 macrophages mediate their anti-C. neoformans activity remains unknown. The current stud","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Dec","modification":"2025-04-04T10:50:19.088Z","creation":"2019-03-27T02:01:58Z"},"accession":"S-EPMC4645398","cross_references":{"pubmed":["26351277"],"doi":["10.1128/iai.00935-15","10.1128/IAI.00935-15"]}}