<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>207(11)</volume><submitter>Me R</submitter><pubmed_abstract>The IL-36 cytokines are known to play various roles in mediating the immune response to infection in a tissue- and pathogen-dependent manner. The present study seeks to investigate the role of IL-36R signaling in C57BL/6 mouse corneas in response to Pseudomonas aeruginosa infection. IL-36α-/-, IL-36γ-/-, and IL-36R-/- mice had significantly more severe keratitis than wild-type mice. At six hours postinfection, IL-36α pretreatment augmented P. aeruginosa-induced expression of IL-1Ra, IL-36γ, LCN2, and S100A8/A9. At one day postinfection, exogenous IL-36α suppressed, whereas IL-36α deficiency promoted, the expression of IL-1β. At three days postinfection, exogenous IL-36α suppressed Th1 but promoted Th2 immune response. IL-36α stimulated the infiltration of IL-22-expressing immune cells, and</pubmed_abstract><journal>Journal of immunology (Baltimore, Md. : 1950)</journal><pagination>2868-2877</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8612993</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>IL-36α Enhances Host Defense against Pseudomonas aeruginosa Keratitis in C57BL/6 Mouse Corneas.</pubmed_title><pmcid>PMC8612993</pmcid><pubmed_authors>Lee PSY</pubmed_authors><pubmed_authors>Gao N</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Standiford TJ</pubmed_authors><pubmed_authors>Mi QS</pubmed_authors><pubmed_authors>Liu T</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Yu FX</pubmed_authors><pubmed_authors>Me R</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-36α Enhances Host Defense against Pseudomonas aeruginosa Keratitis in C57BL/6 Mouse Corneas.</name><description>The IL-36 cytokines are known to play various roles in mediating the immune response to infection in a tissue- and pathogen-dependent manner. The present study seeks to investigate the role of IL-36R signaling in C57BL/6 mouse corneas in response to Pseudomonas aeruginosa infection. IL-36α-/-, IL-36γ-/-, and IL-36R-/- mice had significantly more severe keratitis than wild-type mice. At six hours postinfection, IL-36α pretreatment augmented P. aeruginosa-induced expression of IL-1Ra, IL-36γ, LCN2, and S100A8/A9. At one day postinfection, exogenous IL-36α suppressed, whereas IL-36α deficiency promoted, the expression of IL-1β. At three days postinfection, exogenous IL-36α suppressed Th1 but promoted Th2 immune response. IL-36α stimulated the infiltration of IL-22-expressing immune cells, and</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2025-04-25T20:49:14.108Z</modification><creation>2025-04-06T08:35:10.128Z</creation></dates><accession>S-EPMC8612993</accession><cross_references><pubmed>34686582</pubmed><doi>10.4049/jimmunol.2001246</doi></cross_references></HashMap>