| http://purl.uniprot.org/citations/32295876 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/32295876 | http://www.w3.org/2000/01/rdf-schema#comment | "CD137 modulates type 1 diabetes (T1D) progression in NOD mice. We previously showed that CD137 expression in CD4 T cells inhibits T1D, but its expression in CD8 T cells promotes disease development by intrinsically enhancing the accumulation of β-cell-autoreactive CD8 T cells. CD137 is expressed on a subset of FOXP3+ regulatory CD4 T cells (Tregs), and CD137+ Tregs are the main source of soluble CD137. Soluble CD137 suppresses T cells in vitro by binding to the CD137 ligand (CD137L) upregulated on activated T cells. To further study how the opposing functions of CD137 are regulated, we successfully targeted Tnfsf9 (encoding CD137L) in NOD mice using the CRISPR/Cas9 system (designated NOD.Tnfsf9 -/-). Relative to wild-type NOD mice, T1D development in the NOD.Tnfsf9 -/- strain was significantly delayed, and mice developed less insulitis and had reduced frequencies of β-cell-autoreactive CD8 T cells. Bone marrow chimera experiments showed that CD137L-deficient hematopoietic cells were able to confer T1D resistance. Adoptive T cell transfer experiments showed that CD137L deficiency on myeloid APCs was associated with T1D suppression. Conversely, lack of CD137L on T cells enhanced their diabetogenic activity. Furthermore, neither CD137 nor CD137L was required for the development and homeostasis of FOXP3+ Tregs. However, CD137 was critical for the in vivo T1D-suppressive activity of FOXP3+ Tregs, suggesting that the interaction between CD137 and CD137L regulates their function. Collectively, our results provide new insights into the complex roles of CD137-CD137L interaction in T1D."xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1900485"xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/author | "Chen Y.G."xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/author | "Geurts A.M."xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/author | "Serreze D.V."xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/author | "Ridgway W.M."xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/author | "Ciecko A.E."xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/author | "Foda B.M."xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/pages | "2887-2899"xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/title | "The CD137 Ligand Is Important for Type 1 Diabetes Development but Dispensable for the Homeostasis of Disease-Suppressive CD137+ FOXP3+ Regulatory CD4 T Cells."xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://purl.uniprot.org/core/volume | "204"xsd:string |
| http://purl.uniprot.org/citations/32295876 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/32295876 |
| http://purl.uniprot.org/citations/32295876 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/32295876 |
| http://purl.uniprot.org/uniprot/#_A0A3Q4EC35-mappedCitation-32295876 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/32295876 |
| http://purl.uniprot.org/uniprot/#_A0A3Q4EC46-mappedCitation-32295876 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/32295876 |
| http://purl.uniprot.org/uniprot/#_A0A3Q4EI60-mappedCitation-32295876 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/32295876 |
| http://purl.uniprot.org/uniprot/#_A0A3Q4L2R0-mappedCitation-32295876 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/32295876 |
| http://purl.uniprot.org/uniprot/#_P41274-mappedCitation-32295876 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/32295876 |
| http://purl.uniprot.org/uniprot/#_Q3U1Z9-mappedCitation-32295876 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/32295876 |
| http://purl.uniprot.org/uniprot/#_Q99JB6-mappedCitation-32295876 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/32295876 |
| http://purl.uniprot.org/uniprot/#_V5LWQ0-mappedCitation-32295876 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/32295876 |
| http://purl.uniprot.org/uniprot/#_Q3TEQ6-mappedCitation-32295876 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/32295876 |