<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gong Y</submitter><funding>National Natural Science Foundation of China Youth Projects</funding><funding>Beijing natural science foundation</funding><funding>National Natural Science Foundation of China</funding><funding>Scientific Research Base Construction-Scientific and Technological Innovation Platform Metabolic Disorders Related Cardiovascular Diseases Research Platform Construction</funding><pagination>584-93</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4788697</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>64(2)</volume><pubmed_abstract>Diabetes mellitus is a chronic metabolic disorder with a high morbidity and mortality, but its pathogenesis is not fully understood. An increasing amount of evidence indicates that an immune mechanism plays an important role in the pathogenesis of diabetes. We demonstrated previously that the long-term presence of autoantibodies against the second extracellular loop of the β1-adrenoceptor (β1-AA) could change the ratio of peripheral CD4+T/CD8+T in rats, which was accompanied by lymphocytes infiltration in the rat heart, liver, and kidneys. To investigate whether β1-AA is involved in the pathogenesis of diabetes, BALB/c or nude mice were passively immunized with monoclonal antibodies against β1-AR (β1-AR mAb). Compared with vehicle control mice, β1-AA-positive BALB/c mice exhibited signific</pubmed_abstract><journal>Immunologic research</journal><pubmed_title>Autoantibodies against β1-adrenoceptor induce blood glucose enhancement and insulin insufficient via T lymphocytes.</pubmed_title><pmcid>PMC4788697</pmcid><funding_grant_id>81300694</funding_grant_id><funding_grant_id>PXM2015_014226_000062</funding_grant_id><funding_grant_id>2014CB560700</funding_grant_id><funding_grant_id>7151001</funding_grant_id><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Du Y</pubmed_authors><pubmed_authors>Zhang S</pubmed_authors><pubmed_authors>Gong Y</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors><pubmed_authors>Xiong H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Autoantibodies against β1-adrenoceptor induce blood glucose enhancement and insulin insufficient via T lymphocytes.</name><description>Diabetes mellitus is a chronic metabolic disorder with a high morbidity and mortality, but its pathogenesis is not fully understood. An increasing amount of evidence indicates that an immune mechanism plays an important role in the pathogenesis of diabetes. We demonstrated previously that the long-term presence of autoantibodies against the second extracellular loop of the β1-adrenoceptor (β1-AA) could change the ratio of peripheral CD4+T/CD8+T in rats, which was accompanied by lymphocytes infiltration in the rat heart, liver, and kidneys. To investigate whether β1-AA is involved in the pathogenesis of diabetes, BALB/c or nude mice were passively immunized with monoclonal antibodies against β1-AR (β1-AR mAb). Compared with vehicle control mice, β1-AA-positive BALB/c mice exhibited signific</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Apr</publication><modification>2025-04-18T22:05:16.071Z</modification><creation>2019-03-27T02:10:57Z</creation></dates><accession>S-EPMC4788697</accession><cross_references><pubmed>26639354</pubmed><doi>10.1007/s12026-015-8757-7</doi></cross_references></HashMap>