http://purl.uniprot.org/citations/32513716 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/32513716 | http://www.w3.org/2000/01/rdf-schema#comment | "Immature T cells undergo a process of positive selection in the thymus when their new T cell receptor (TCR) engages and signals in response to self-peptides. As the T cell matures, a slew of negative regulatory molecules, including the inhibitory surface glycoprotein CD5, are up-regulated in proportion to the strength of the self-peptide signal. Together these regulators dampen TCR-proximal signaling and help avoid any subsequent peripheral activation of T cells by self-peptides. Paradoxically, antigen-specific T cells initially expressing more CD5 (CD5hi) have been found to better persist as effector/memory cells after a peripheral challenge. The molecular mechanisms underlying such a duality in CD5 function is not clear. We found that CD5 alters the basal activity of the NF-κB signaling in resting peripheral T cells. When CD5 was conditionally ablated, T cells were unable to maintain higher expression of the cytoplasmic NF-κB inhibitor IκBα. Consistent with this, resting CD5hi T cells expressed more of the NF-κB p65 protein than CD5lo cells, without significant increases in transcript levels, in the absence of TCR signals. This posttranslationally stabilized cellular NF-κB depot potentially confers a survival advantage to CD5hi T cells over CD5lo ones. Taken together, these data suggest a two-step model whereby the strength of self-peptide-induced TCR signal lead to the up-regulation of CD5, which subsequently maintains a proportional reserve of NF-κB in peripheral T cells poised for responding to agonistic antigen-driven T cell activation."xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.1922525117"xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/author | "Choi S."xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/author | "Zhao B."xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/author | "Mitra A."xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/author | "Love P.E."xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/author | "Livak F."xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/author | "Singh N.J."xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/author | "Matson C.A."xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/pages | "14342-14353"xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/title | "CD5 dynamically calibrates basal NF-kappaB signaling in T cells during thymic development and peripheral activation."xsd:string |
http://purl.uniprot.org/citations/32513716 | http://purl.uniprot.org/core/volume | "117"xsd:string |
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