| http://purl.uniprot.org/citations/23536631 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23536631 | http://www.w3.org/2000/01/rdf-schema#comment | "The TNFR family member 4-1BB plays a key role in the survival of activated and memory CD8 T cells. However, the mechanisms that regulate 4-1BB re-expression on memory CD8 T cells after Ag clearance are unknown. In unimmunized mice, ∼10% of CD8 CD44(hi) memory T cells in the bone marrow (BM) and liver express 4-1BB, with minimal 4-1BB expression in spleen and lymph node. IL-2, IL-15, and IL-7 are collectively dispensable for 4-1BB expression on the memory CD8 T cells. Rather, T cell-intrinsic glucocorticoid-induced TNFR-related protein (GITR) contributes to 4-1BB expression on CD8 T cells upon their entry into the BM or liver. Consistent with its role in regulation of 4-1BB, GITR is required on memory CD8 T cells for their persistence in vivo. These findings reveal site-specific effects of the BM and liver microenvironment on CD8 memory T cells. Previous work has demonstrated that 4-1BB agonists given to unimmunized mice induce splenomegaly, hepatitis, and other immune system anomalies. Moreover, severe liver pathology has been observed in a subset of anti-4-1BB-treated melanoma patients. Remarkably, the absence of GITR in mice almost completely abrogates cellular expansions, splenomegaly, and liver inflammation associated with anti-4-1BB agonist treatment of unimmunized mice. In contrast, lack of CD8 T cells selectively improves liver pathology, but not splenomegaly in the mice. Thus, the regulation of 4-1BB expression by GITR on CD8 T cells, as well as on other cells, contributes to the pathological effects of anti-4-1BB in unimmunized mice."xsd:string |
| http://purl.uniprot.org/citations/23536631 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1201854"xsd:string |
| http://purl.uniprot.org/citations/23536631 | http://purl.uniprot.org/core/author | "Watts T.H."xsd:string |
| http://purl.uniprot.org/citations/23536631 | http://purl.uniprot.org/core/author | "Lin G.H."xsd:string |
| http://purl.uniprot.org/citations/23536631 | http://purl.uniprot.org/core/author | "Snell L.M."xsd:string |
| http://purl.uniprot.org/citations/23536631 | http://purl.uniprot.org/core/author | "Wortzman M.E."xsd:string |
| http://purl.uniprot.org/citations/23536631 | http://purl.uniprot.org/core/author | "Clouthier D.L."xsd:string |
| http://purl.uniprot.org/citations/23536631 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23536631 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/23536631 | http://purl.uniprot.org/core/pages | "4627-4639"xsd:string |
| http://purl.uniprot.org/citations/23536631 | http://purl.uniprot.org/core/title | "GITR-dependent regulation of 4-1BB expression: implications for T cell memory and anti-4-1BB-induced pathology."xsd:string |
| http://purl.uniprot.org/citations/23536631 | http://purl.uniprot.org/core/volume | "190"xsd:string |
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