PMC:7417788 / 26097-27296 JSONTXT

{"project":"LitCovid-PMC-OGER-BB","denotations":[{"id":"T612","span":{"begin":38,"end":43},"obj":"GO:0007568"},{"id":"T613","span":{"begin":292,"end":298},"obj":"PR:P25859"},{"id":"T614","span":{"begin":305,"end":315},"obj":"GO:0010467"},{"id":"T615","span":{"begin":329,"end":333},"obj":"PR:P24100"},{"id":"T616","span":{"begin":351,"end":358},"obj":"CHEBI:59132;CHEBI:59132;GO:0019882"},{"id":"T617","span":{"begin":359,"end":371},"obj":"GO:0019882"},{"id":"T618","span":{"begin":380,"end":385},"obj":"SO:0000704"},{"id":"T619","span":{"begin":394,"end":397},"obj":"PR:000003858"},{"id":"T620","span":{"begin":399,"end":405},"obj":"PR:000005570"},{"id":"T621","span":{"begin":411,"end":418},"obj":"PR:000005559"},{"id":"T622","span":{"begin":432,"end":442},"obj":"GO:0010467"},{"id":"T623","span":{"begin":456,"end":460},"obj":"PR:P25859"},{"id":"T624","span":{"begin":461,"end":468},"obj":"CL:0000236"},{"id":"T625","span":{"begin":495,"end":500},"obj":"GO:0007568"},{"id":"T626","span":{"begin":512,"end":517},"obj":"SO:0000704"},{"id":"T627","span":{"begin":541,"end":546},"obj":"SO:0000704"},{"id":"T628","span":{"begin":548,"end":552},"obj":"PR:000001136"},{"id":"T629","span":{"begin":554,"end":560},"obj":"PR:000005279"},{"id":"T630","span":{"begin":562,"end":567},"obj":"PR:000006348"},{"id":"T631","span":{"begin":569,"end":574},"obj":"PR:000001395"},{"id":"T632","span":{"begin":580,"end":585},"obj":"PR:000006746"},{"id":"T633","span":{"begin":700,"end":704},"obj":"PR:P24100"},{"id":"T634","span":{"begin":718,"end":724},"obj":"UBERON:0002405"},{"id":"T635","span":{"begin":725,"end":735},"obj":"GO:0065007"},{"id":"T636","span":{"begin":740,"end":747},"obj":"CHEBI:59132;CHEBI:59132;GO:0019882"},{"id":"T637","span":{"begin":748,"end":760},"obj":"GO:0019882"},{"id":"T638","span":{"begin":777,"end":782},"obj":"GO:0007568"},{"id":"T639","span":{"begin":791,"end":797},"obj":"PR:P25859"},{"id":"T640","span":{"begin":808,"end":816},"obj":"PR:000002014"},{"id":"T641","span":{"begin":817,"end":827},"obj":"GO:0010467"},{"id":"T642","span":{"begin":969,"end":976},"obj":"PR:000005559"},{"id":"T643","span":{"begin":1002,"end":1007},"obj":"GO:0007568"},{"id":"T644","span":{"begin":1079,"end":1084},"obj":"GO:0007568"},{"id":"T645","span":{"begin":1097,"end":1104},"obj":"CHEBI:59132;CHEBI:59132;GO:0019882"},{"id":"T646","span":{"begin":1105,"end":1117},"obj":"GO:0019882"},{"id":"T647","span":{"begin":1159,"end":1164},"obj":"GO:0007568"},{"id":"T648","span":{"begin":1176,"end":1180},"obj":"SO:0000704;GO:0010467"},{"id":"T649","span":{"begin":1181,"end":1191},"obj":"GO:0010467"}],"text":"Within DC clusters, we found distinct aging manifestations in the cDC2 subsets by comparing DC clusters in the t-SNE map (Fig. 3J). Cells from the YA group grouped together in clusters 0 and 1 (named cDC2-A), whereas cells in AA group grouped distinctively in clusters 3, 4, 10 and 11 (named cDC2-B). The expression signature of cDC2-A cells included antigen presentation-related genes such as AHR, CLEC4E, and CLEC12A, whereas the expression signature of cDC2-B cells included inflammatory and aging-associated genes such as IFN-stimulated genes, IL1B, CDKN2D, DDIT4, CXCL8, and DUSP2 (Fig. S7J and S7K). Moreover, the comparative functional analysis of DEGs between the two clusters indicated that cDC2-A had intact immune regulation and antigen presentation function, while aging-related cDC2-B with high HLA-DQA2 expression exhibited increased inflammatory signaling pathways, such as the response to hypoxia and IL-1 signaling (Fig. 3K). We further confirmed that CLEC12A+ cDC2s were decreased in aging by FACS (Fig. 3L and 3M). Taken together, these findings indicate that aging curtails DC antigen presentation ability and upregulates inflammatory and aging-associated gene expression in DCs."}

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T236","span":{"begin":117,"end":120},"obj":"Body_part"},{"id":"T237","span":{"begin":132,"end":137},"obj":"Body_part"},{"id":"T238","span":{"begin":217,"end":222},"obj":"Body_part"},{"id":"T239","span":{"begin":336,"end":341},"obj":"Body_part"},{"id":"T240","span":{"begin":463,"end":468},"obj":"Body_part"},{"id":"T241","span":{"begin":808,"end":811},"obj":"Body_part"},{"id":"T242","span":{"begin":917,"end":921},"obj":"Body_part"},{"id":"T243","span":{"begin":917,"end":919},"obj":"Body_part"},{"id":"T244","span":{"begin":1176,"end":1180},"obj":"Body_part"}],"attributes":[{"id":"A236","pred":"fma_id","subj":"T236","obj":"http://purl.org/sig/ont/fma/fma67847"},{"id":"A237","pred":"fma_id","subj":"T237","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A238","pred":"fma_id","subj":"T238","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A239","pred":"fma_id","subj":"T239","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A240","pred":"fma_id","subj":"T240","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A241","pred":"fma_id","subj":"T241","obj":"http://purl.org/sig/ont/fma/fma84795"},{"id":"A242","pred":"fma_id","subj":"T242","obj":"http://purl.org/sig/ont/fma/fma86583"},{"id":"A243","pred":"fma_id","subj":"T243","obj":"http://purl.org/sig/ont/fma/fma86578"},{"id":"A244","pred":"fma_id","subj":"T244","obj":"http://purl.org/sig/ont/fma/fma74402"}],"text":"Within DC clusters, we found distinct aging manifestations in the cDC2 subsets by comparing DC clusters in the t-SNE map (Fig. 3J). Cells from the YA group grouped together in clusters 0 and 1 (named cDC2-A), whereas cells in AA group grouped distinctively in clusters 3, 4, 10 and 11 (named cDC2-B). The expression signature of cDC2-A cells included antigen presentation-related genes such as AHR, CLEC4E, and CLEC12A, whereas the expression signature of cDC2-B cells included inflammatory and aging-associated genes such as IFN-stimulated genes, IL1B, CDKN2D, DDIT4, CXCL8, and DUSP2 (Fig. S7J and S7K). Moreover, the comparative functional analysis of DEGs between the two clusters indicated that cDC2-A had intact immune regulation and antigen presentation function, while aging-related cDC2-B with high HLA-DQA2 expression exhibited increased inflammatory signaling pathways, such as the response to hypoxia and IL-1 signaling (Fig. 3K). We further confirmed that CLEC12A+ cDC2s were decreased in aging by FACS (Fig. 3L and 3M). Taken together, these findings indicate that aging curtails DC antigen presentation ability and upregulates inflammatory and aging-associated gene expression in DCs."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T45","span":{"begin":113,"end":116},"obj":"Disease"},{"id":"T46","span":{"begin":1011,"end":1015},"obj":"Disease"}],"attributes":[{"id":"A45","pred":"mondo_id","subj":"T45","obj":"http://purl.obolibrary.org/obo/MONDO_0018859"},{"id":"A46","pred":"mondo_id","subj":"T46","obj":"http://purl.obolibrary.org/obo/MONDO_0018262"}],"text":"Within DC clusters, we found distinct aging manifestations in the cDC2 subsets by comparing DC clusters in the t-SNE map (Fig. 3J). Cells from the YA group grouped together in clusters 0 and 1 (named cDC2-A), whereas cells in AA group grouped distinctively in clusters 3, 4, 10 and 11 (named cDC2-B). The expression signature of cDC2-A cells included antigen presentation-related genes such as AHR, CLEC4E, and CLEC12A, whereas the expression signature of cDC2-B cells included inflammatory and aging-associated genes such as IFN-stimulated genes, IL1B, CDKN2D, DDIT4, CXCL8, and DUSP2 (Fig. S7J and S7K). Moreover, the comparative functional analysis of DEGs between the two clusters indicated that cDC2-A had intact immune regulation and antigen presentation function, while aging-related cDC2-B with high HLA-DQA2 expression exhibited increased inflammatory signaling pathways, such as the response to hypoxia and IL-1 signaling (Fig. 3K). We further confirmed that CLEC12A+ cDC2s were decreased in aging by FACS (Fig. 3L and 3M). Taken together, these findings indicate that aging curtails DC antigen presentation ability and upregulates inflammatory and aging-associated gene expression in DCs."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T511","span":{"begin":132,"end":137},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T512","span":{"begin":205,"end":206},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T513","span":{"begin":217,"end":222},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T514","span":{"begin":226,"end":228},"obj":"http://purl.obolibrary.org/obo/CLO_0001627"},{"id":"T515","span":{"begin":269,"end":273},"obj":"http://purl.obolibrary.org/obo/CLO_0001302"},{"id":"T516","span":{"begin":282,"end":284},"obj":"http://purl.obolibrary.org/obo/CLO_0053733"},{"id":"T517","span":{"begin":297,"end":298},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T518","span":{"begin":334,"end":335},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T519","span":{"begin":336,"end":341},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T520","span":{"begin":380,"end":385},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T521","span":{"begin":461,"end":468},"obj":"http://purl.obolibrary.org/obo/CL_0000236"},{"id":"T522","span":{"begin":512,"end":517},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T523","span":{"begin":541,"end":546},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T524","span":{"begin":548,"end":552},"obj":"http://purl.obolibrary.org/obo/PR_000001136"},{"id":"T525","span":{"begin":705,"end":706},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T526","span":{"begin":796,"end":797},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T527","span":{"begin":861,"end":870},"obj":"http://purl.obolibrary.org/obo/SO_0000418"},{"id":"T528","span":{"begin":922,"end":931},"obj":"http://purl.obolibrary.org/obo/SO_0000418"},{"id":"T529","span":{"begin":1176,"end":1180},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T530","span":{"begin":1195,"end":1198},"obj":"http://purl.obolibrary.org/obo/CL_0000451"}],"text":"Within DC clusters, we found distinct aging manifestations in the cDC2 subsets by comparing DC clusters in the t-SNE map (Fig. 3J). Cells from the YA group grouped together in clusters 0 and 1 (named cDC2-A), whereas cells in AA group grouped distinctively in clusters 3, 4, 10 and 11 (named cDC2-B). The expression signature of cDC2-A cells included antigen presentation-related genes such as AHR, CLEC4E, and CLEC12A, whereas the expression signature of cDC2-B cells included inflammatory and aging-associated genes such as IFN-stimulated genes, IL1B, CDKN2D, DDIT4, CXCL8, and DUSP2 (Fig. S7J and S7K). Moreover, the comparative functional analysis of DEGs between the two clusters indicated that cDC2-A had intact immune regulation and antigen presentation function, while aging-related cDC2-B with high HLA-DQA2 expression exhibited increased inflammatory signaling pathways, such as the response to hypoxia and IL-1 signaling (Fig. 3K). We further confirmed that CLEC12A+ cDC2s were decreased in aging by FACS (Fig. 3L and 3M). Taken together, these findings indicate that aging curtails DC antigen presentation ability and upregulates inflammatory and aging-associated gene expression in DCs."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T163","span":{"begin":147,"end":149},"obj":"Chemical"},{"id":"T164","span":{"begin":150,"end":155},"obj":"Chemical"},{"id":"T165","span":{"begin":226,"end":228},"obj":"Chemical"},{"id":"T167","span":{"begin":229,"end":234},"obj":"Chemical"},{"id":"T168","span":{"begin":351,"end":358},"obj":"Chemical"},{"id":"T169","span":{"begin":740,"end":747},"obj":"Chemical"},{"id":"T170","span":{"begin":917,"end":919},"obj":"Chemical"},{"id":"T172","span":{"begin":1097,"end":1104},"obj":"Chemical"}],"attributes":[{"id":"A163","pred":"chebi_id","subj":"T163","obj":"http://purl.obolibrary.org/obo/CHEBI_74879"},{"id":"A164","pred":"chebi_id","subj":"T164","obj":"http://purl.obolibrary.org/obo/CHEBI_24433"},{"id":"A165","pred":"chebi_id","subj":"T165","obj":"http://purl.obolibrary.org/obo/CHEBI_15843"},{"id":"A166","pred":"chebi_id","subj":"T165","obj":"http://purl.obolibrary.org/obo/CHEBI_72816"},{"id":"A167","pred":"chebi_id","subj":"T167","obj":"http://purl.obolibrary.org/obo/CHEBI_24433"},{"id":"A168","pred":"chebi_id","subj":"T168","obj":"http://purl.obolibrary.org/obo/CHEBI_59132"},{"id":"A169","pred":"chebi_id","subj":"T169","obj":"http://purl.obolibrary.org/obo/CHEBI_59132"},{"id":"A170","pred":"chebi_id","subj":"T170","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A171","pred":"chebi_id","subj":"T170","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A172","pred":"chebi_id","subj":"T172","obj":"http://purl.obolibrary.org/obo/CHEBI_59132"}],"text":"Within DC clusters, we found distinct aging manifestations in the cDC2 subsets by comparing DC clusters in the t-SNE map (Fig. 3J). Cells from the YA group grouped together in clusters 0 and 1 (named cDC2-A), whereas cells in AA group grouped distinctively in clusters 3, 4, 10 and 11 (named cDC2-B). The expression signature of cDC2-A cells included antigen presentation-related genes such as AHR, CLEC4E, and CLEC12A, whereas the expression signature of cDC2-B cells included inflammatory and aging-associated genes such as IFN-stimulated genes, IL1B, CDKN2D, DDIT4, CXCL8, and DUSP2 (Fig. S7J and S7K). Moreover, the comparative functional analysis of DEGs between the two clusters indicated that cDC2-A had intact immune regulation and antigen presentation function, while aging-related cDC2-B with high HLA-DQA2 expression exhibited increased inflammatory signaling pathways, such as the response to hypoxia and IL-1 signaling (Fig. 3K). We further confirmed that CLEC12A+ cDC2s were decreased in aging by FACS (Fig. 3L and 3M). Taken together, these findings indicate that aging curtails DC antigen presentation ability and upregulates inflammatory and aging-associated gene expression in DCs."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T139","span":{"begin":38,"end":43},"obj":"http://purl.obolibrary.org/obo/GO_0007568"},{"id":"T140","span":{"begin":351,"end":371},"obj":"http://purl.obolibrary.org/obo/GO_0019882"},{"id":"T141","span":{"begin":495,"end":500},"obj":"http://purl.obolibrary.org/obo/GO_0007568"},{"id":"T142","span":{"begin":725,"end":735},"obj":"http://purl.obolibrary.org/obo/GO_0065007"},{"id":"T143","span":{"begin":740,"end":760},"obj":"http://purl.obolibrary.org/obo/GO_0019882"},{"id":"T144","span":{"begin":777,"end":782},"obj":"http://purl.obolibrary.org/obo/GO_0007568"},{"id":"T145","span":{"begin":861,"end":879},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T146","span":{"begin":861,"end":870},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T147","span":{"begin":893,"end":912},"obj":"http://purl.obolibrary.org/obo/GO_0001666"},{"id":"T148","span":{"begin":922,"end":931},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T149","span":{"begin":1002,"end":1007},"obj":"http://purl.obolibrary.org/obo/GO_0007568"},{"id":"T150","span":{"begin":1079,"end":1084},"obj":"http://purl.obolibrary.org/obo/GO_0007568"},{"id":"T151","span":{"begin":1097,"end":1117},"obj":"http://purl.obolibrary.org/obo/GO_0019882"},{"id":"T152","span":{"begin":1159,"end":1164},"obj":"http://purl.obolibrary.org/obo/GO_0007568"},{"id":"T153","span":{"begin":1176,"end":1191},"obj":"http://purl.obolibrary.org/obo/GO_0010467"}],"text":"Within DC clusters, we found distinct aging manifestations in the cDC2 subsets by comparing DC clusters in the t-SNE map (Fig. 3J). Cells from the YA group grouped together in clusters 0 and 1 (named cDC2-A), whereas cells in AA group grouped distinctively in clusters 3, 4, 10 and 11 (named cDC2-B). The expression signature of cDC2-A cells included antigen presentation-related genes such as AHR, CLEC4E, and CLEC12A, whereas the expression signature of cDC2-B cells included inflammatory and aging-associated genes such as IFN-stimulated genes, IL1B, CDKN2D, DDIT4, CXCL8, and DUSP2 (Fig. S7J and S7K). Moreover, the comparative functional analysis of DEGs between the two clusters indicated that cDC2-A had intact immune regulation and antigen presentation function, while aging-related cDC2-B with high HLA-DQA2 expression exhibited increased inflammatory signaling pathways, such as the response to hypoxia and IL-1 signaling (Fig. 3K). We further confirmed that CLEC12A+ cDC2s were decreased in aging by FACS (Fig. 3L and 3M). Taken together, these findings indicate that aging curtails DC antigen presentation ability and upregulates inflammatory and aging-associated gene expression in DCs."}

{"project":"LitCovid-sentences","denotations":[{"id":"T131","span":{"begin":0,"end":131},"obj":"Sentence"},{"id":"T132","span":{"begin":132,"end":300},"obj":"Sentence"},{"id":"T133","span":{"begin":301,"end":605},"obj":"Sentence"},{"id":"T134","span":{"begin":606,"end":942},"obj":"Sentence"},{"id":"T135","span":{"begin":943,"end":1033},"obj":"Sentence"},{"id":"T136","span":{"begin":1034,"end":1199},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Within DC clusters, we found distinct aging manifestations in the cDC2 subsets by comparing DC clusters in the t-SNE map (Fig. 3J). Cells from the YA group grouped together in clusters 0 and 1 (named cDC2-A), whereas cells in AA group grouped distinctively in clusters 3, 4, 10 and 11 (named cDC2-B). The expression signature of cDC2-A cells included antigen presentation-related genes such as AHR, CLEC4E, and CLEC12A, whereas the expression signature of cDC2-B cells included inflammatory and aging-associated genes such as IFN-stimulated genes, IL1B, CDKN2D, DDIT4, CXCL8, and DUSP2 (Fig. S7J and S7K). Moreover, the comparative functional analysis of DEGs between the two clusters indicated that cDC2-A had intact immune regulation and antigen presentation function, while aging-related cDC2-B with high HLA-DQA2 expression exhibited increased inflammatory signaling pathways, such as the response to hypoxia and IL-1 signaling (Fig. 3K). We further confirmed that CLEC12A+ cDC2s were decreased in aging by FACS (Fig. 3L and 3M). Taken together, these findings indicate that aging curtails DC antigen presentation ability and upregulates inflammatory and aging-associated gene expression in DCs."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T6","span":{"begin":905,"end":912},"obj":"Phenotype"}],"attributes":[{"id":"A6","pred":"hp_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/HP_0012418"}],"text":"Within DC clusters, we found distinct aging manifestations in the cDC2 subsets by comparing DC clusters in the t-SNE map (Fig. 3J). Cells from the YA group grouped together in clusters 0 and 1 (named cDC2-A), whereas cells in AA group grouped distinctively in clusters 3, 4, 10 and 11 (named cDC2-B). The expression signature of cDC2-A cells included antigen presentation-related genes such as AHR, CLEC4E, and CLEC12A, whereas the expression signature of cDC2-B cells included inflammatory and aging-associated genes such as IFN-stimulated genes, IL1B, CDKN2D, DDIT4, CXCL8, and DUSP2 (Fig. S7J and S7K). Moreover, the comparative functional analysis of DEGs between the two clusters indicated that cDC2-A had intact immune regulation and antigen presentation function, while aging-related cDC2-B with high HLA-DQA2 expression exhibited increased inflammatory signaling pathways, such as the response to hypoxia and IL-1 signaling (Fig. 3K). We further confirmed that CLEC12A+ cDC2s were decreased in aging by FACS (Fig. 3L and 3M). Taken together, these findings indicate that aging curtails DC antigen presentation ability and upregulates inflammatory and aging-associated gene expression in DCs."}

{"project":"LitCovid-PubTator","denotations":[{"id":"590","span":{"begin":66,"end":70},"obj":"Gene"},{"id":"591","span":{"begin":394,"end":397},"obj":"Gene"},{"id":"592","span":{"begin":399,"end":405},"obj":"Gene"},{"id":"593","span":{"begin":411,"end":418},"obj":"Gene"},{"id":"594","span":{"begin":548,"end":552},"obj":"Gene"},{"id":"595","span":{"begin":554,"end":560},"obj":"Gene"},{"id":"596","span":{"begin":562,"end":567},"obj":"Gene"},{"id":"597","span":{"begin":569,"end":574},"obj":"Gene"},{"id":"598","span":{"begin":580,"end":585},"obj":"Gene"},{"id":"599","span":{"begin":808,"end":816},"obj":"Gene"},{"id":"600","span":{"begin":917,"end":921},"obj":"Gene"},{"id":"601","span":{"begin":969,"end":976},"obj":"Gene"},{"id":"602","span":{"begin":978,"end":982},"obj":"Gene"},{"id":"603","span":{"begin":329,"end":333},"obj":"Gene"},{"id":"604","span":{"begin":526,"end":529},"obj":"Gene"},{"id":"605","span":{"begin":905,"end":912},"obj":"Disease"}],"attributes":[{"id":"A590","pred":"tao:has_database_id","subj":"590","obj":"Gene:983"},{"id":"A591","pred":"tao:has_database_id","subj":"591","obj":"Gene:196"},{"id":"A592","pred":"tao:has_database_id","subj":"592","obj":"Gene:26253"},{"id":"A593","pred":"tao:has_database_id","subj":"593","obj":"Gene:160364"},{"id":"A594","pred":"tao:has_database_id","subj":"594","obj":"Gene:3553"},{"id":"A595","pred":"tao:has_database_id","subj":"595","obj":"Gene:1032"},{"id":"A596","pred":"tao:has_database_id","subj":"596","obj":"Gene:54541"},{"id":"A597","pred":"tao:has_database_id","subj":"597","obj":"Gene:3576"},{"id":"A598","pred":"tao:has_database_id","subj":"598","obj":"Gene:1844"},{"id":"A599","pred":"tao:has_database_id","subj":"599","obj":"Gene:3118"},{"id":"A600","pred":"tao:has_database_id","subj":"600","obj":"Gene:3553"},{"id":"A601","pred":"tao:has_database_id","subj":"601","obj":"Gene:160364"},{"id":"A602","pred":"tao:has_database_id","subj":"602","obj":"Gene:983"},{"id":"A603","pred":"tao:has_database_id","subj":"603","obj":"Gene:983"},{"id":"A604","pred":"tao:has_database_id","subj":"604","obj":"Gene:3439"},{"id":"A605","pred":"tao:has_database_id","subj":"605","obj":"MESH:D000860"}],"namespaces":[{"prefix":"Tax","uri":"https://www.ncbi.nlm.nih.gov/taxonomy/"},{"prefix":"MESH","uri":"https://id.nlm.nih.gov/mesh/"},{"prefix":"Gene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"CVCL","uri":"https://web.expasy.org/cellosaurus/CVCL_"}],"text":"Within DC clusters, we found distinct aging manifestations in the cDC2 subsets by comparing DC clusters in the t-SNE map (Fig. 3J). Cells from the YA group grouped together in clusters 0 and 1 (named cDC2-A), whereas cells in AA group grouped distinctively in clusters 3, 4, 10 and 11 (named cDC2-B). The expression signature of cDC2-A cells included antigen presentation-related genes such as AHR, CLEC4E, and CLEC12A, whereas the expression signature of cDC2-B cells included inflammatory and aging-associated genes such as IFN-stimulated genes, IL1B, CDKN2D, DDIT4, CXCL8, and DUSP2 (Fig. S7J and S7K). Moreover, the comparative functional analysis of DEGs between the two clusters indicated that cDC2-A had intact immune regulation and antigen presentation function, while aging-related cDC2-B with high HLA-DQA2 expression exhibited increased inflammatory signaling pathways, such as the response to hypoxia and IL-1 signaling (Fig. 3K). We further confirmed that CLEC12A+ cDC2s were decreased in aging by FACS (Fig. 3L and 3M). Taken together, these findings indicate that aging curtails DC antigen presentation ability and upregulates inflammatory and aging-associated gene expression in DCs."}