{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Maine CJ"],"funding":["NIAID NIH HHS","Wellcome Trust"],"pagination":["5267-75"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3358490"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["188(11)"],"pubmed_abstract":["PTPN22 encodes a tyrosine phosphatase that inhibits Src-family kinases responsible for Ag receptor signaling in lymphocytes and is strongly linked with susceptibility to a number of autoimmune diseases. As strength of TCR signal is critical to the thymic selection of regulatory T cells (Tregs), we examined the effect of murine PTPN22 deficiency on Treg development and function. In the thymus, numbers of pre-Tregs and Tregs increased inversely with the level of PTPN22. This increase in Tregs persisted in the periphery and could play a key part in the reduced severity observed in the PTPN22-deficient mice of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. This could explain the lack of association of certain autoimmune conditions with PTPN22 risk alleles."],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["PTPN22 alters the development of regulatory T cells in the thymus."],"pmcid":["PMC3358490"],"funding_grant_id":["U01 AI070351-04S1","U19 AI050864","5R01AI070544","AI070351","079895","091157","U01 AI070351","U01 AI070351-04","AI050864","R01 AI070544","U01 AI070351-05S1","U01 AI070351-05"],"pubmed_authors":["Wicker LS","Bottini N","Stanford SM","Maine CJ","Cheung J","Hamilton-Williams EE","Sherman LA"],"additional_accession":[]},"is_claimable":false,"name":"PTPN22 alters the development of regulatory T cells in the thymus.","description":"PTPN22 encodes a tyrosine phosphatase that inhibits Src-family kinases responsible for Ag receptor signaling in lymphocytes and is strongly linked with susceptibility to a number of autoimmune diseases. As strength of TCR signal is critical to the thymic selection of regulatory T cells (Tregs), we examined the effect of murine PTPN22 deficiency on Treg development and function. In the thymus, numbers of pre-Tregs and Tregs increased inversely with the level of PTPN22. This increase in Tregs persisted in the periphery and could play a key part in the reduced severity observed in the PTPN22-deficient mice of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. This could explain the lack of association of certain autoimmune conditions with PTPN22 risk alleles.","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Jun","modification":"2020-10-29T14:10:33Z","creation":"2019-03-26T23:42:57Z"},"accession":"S-EPMC3358490","cross_references":{"pubmed":["22539785"],"doi":["10.4049/jimmunol.1200150"]}}