<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Prado MKB</submitter><funding>Conselho Nacional de Desenvolvimento Científico e Tecnológico</funding><funding>Coordenação de Aperfeiçoamento de Pessoal de Nível Superior</funding><funding>Fundação de Amparo à Pesquisa do Estado de São Paulo</funding><pagination>E865</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7356283</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(6)</volume><pubmed_abstract>&lt;i>Histoplasma capsulatum&lt;/i> is the agent of histoplasmosis, one of the most frequent mycoses in the world. The infection initiates with fungal spore inhalation, transformation into yeasts in the lungs and establishment of a granulomatous disease, which is characterized by a Th1 response. The production of Th1 signature cytokines, such as IFN-γ, is crucial for yeast clearance from the lungs, and to prevent dissemination. Recently, it was demonstrated that IL-17, a Th17 signature cytokine, is also important for fungal control, particularly in the absence of Th1 response. IL-22 is another cytokine with multiple functions on host response and disease progression. However, little is known about the role of IL-22 during histoplasmosis. In this study, we demonstrated that absence of IL-22 affec</pubmed_abstract><journal>Biomolecules</journal><pubmed_title>IL-22 Promotes IFN-γ-Mediated Immunity against &lt;i>Histoplasma capsulatum&lt;/i> Infection.</pubmed_title><pmcid>PMC7356283</pmcid><funding_grant_id>Finance Code 001</funding_grant_id><funding_grant_id>302514/2015-5</funding_grant_id><funding_grant_id>2014/07125-6 and 2015/00658-1</funding_grant_id><pubmed_authors>Fontanari C</pubmed_authors><pubmed_authors>Souza COS</pubmed_authors><pubmed_authors>Zoccal KF</pubmed_authors><pubmed_authors>Meirelles AFG</pubmed_authors><pubmed_authors>Prado MKB</pubmed_authors><pubmed_authors>Ramos SG</pubmed_authors><pubmed_authors>Alves-Filho JC</pubmed_authors><pubmed_authors>Faccioli LH</pubmed_authors><pubmed_authors>Gardinassi LG</pubmed_authors><pubmed_authors>Peti APF</pubmed_authors><pubmed_authors>de Paula-Silva FWG</pubmed_authors><pubmed_authors>Sorgi CA</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-22 Promotes IFN-γ-Mediated Immunity against &lt;i>Histoplasma capsulatum&lt;/i> Infection.</name><description>&lt;i>Histoplasma capsulatum&lt;/i> is the agent of histoplasmosis, one of the most frequent mycoses in the world. The infection initiates with fungal spore inhalation, transformation into yeasts in the lungs and establishment of a granulomatous disease, which is characterized by a Th1 response. The production of Th1 signature cytokines, such as IFN-γ, is crucial for yeast clearance from the lungs, and to prevent dissemination. Recently, it was demonstrated that IL-17, a Th17 signature cytokine, is also important for fungal control, particularly in the absence of Th1 response. IL-22 is another cytokine with multiple functions on host response and disease progression. However, little is known about the role of IL-22 during histoplasmosis. In this study, we demonstrated that absence of IL-22 affec</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jun</publication><modification>2025-04-26T07:09:02.119Z</modification><creation>2025-04-06T12:10:32.181Z</creation></dates><accession>S-EPMC7356283</accession><cross_references><pubmed>32517114</pubmed><doi>10.3390/biom10060865</doi></cross_references></HashMap>