<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>16</volume><submitter>Czaran D</submitter><pubmed_abstract>&lt;h4>Objective&lt;/h4>Contact hypersensitivity (CHS), or allergic contact dermatitis (ACD), is an inflammatory skin disorder characterized by an exaggerated allergic reaction to specific haptens. During this delayed-type allergic reaction, the first contact with the allergen initiates the sensitization phase, forming memory T cells. Upon repeated contact with the hapten, the elicitation phase develops, activating mostly macrophages, cytotoxic T cells, and neutrophilic granulocytes. Our group previously demonstrated that the leukocyte-specific GTPase-activating protein ARHGAP25 regulates phagocyte effector functions and is crucial in the pathomechanism of autoantibody-induced arthritis. Here, we investigate its role in the pathogenesis of the more complex inflammatory process of contact hyperse</pubmed_abstract><journal>Frontiers in immunology</journal><pagination>1509713</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11896868</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>ARHGAP25: a novel player in the Pathomechanism of allergic contact hypersensitivity.</pubmed_title><pmcid>PMC11896868</pmcid><pubmed_authors>Sasvari P</pubmed_authors><pubmed_authors>Csepanyi-Komi R</pubmed_authors><pubmed_authors>Lorincz K</pubmed_authors><pubmed_authors>Ella K</pubmed_authors><pubmed_authors>Czaran D</pubmed_authors><pubmed_authors>Gellen V</pubmed_authors></additional><is_claimable>false</is_claimable><name>ARHGAP25: a novel player in the Pathomechanism of allergic contact hypersensitivity.</name><description>&lt;h4>Objective&lt;/h4>Contact hypersensitivity (CHS), or allergic contact dermatitis (ACD), is an inflammatory skin disorder characterized by an exaggerated allergic reaction to specific haptens. During this delayed-type allergic reaction, the first contact with the allergen initiates the sensitization phase, forming memory T cells. Upon repeated contact with the hapten, the elicitation phase develops, activating mostly macrophages, cytotoxic T cells, and neutrophilic granulocytes. Our group previously demonstrated that the leukocyte-specific GTPase-activating protein ARHGAP25 regulates phagocyte effector functions and is crucial in the pathomechanism of autoantibody-induced arthritis. Here, we investigate its role in the pathogenesis of the more complex inflammatory process of contact hyperse</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2025-04-04T01:41:23.631Z</modification><creation>2025-04-04T01:41:23.631Z</creation></dates><accession>S-EPMC11896868</accession><cross_references><pubmed>40078992</pubmed><doi>10.3389/fimmu.2025.1509713</doi></cross_references></HashMap>