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This research investigates the potential of aberrant signatures on T cell genes, soluble Co-IRs\/ligands, and Co-IRs expression on T cells as biomarkers for lupus disease parameters.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Comparative transcriptome profiling analysis of non-renal and end-stage renal disease (ESRD) phenotypes of SLE was performed using CD4\u2009+\u2009and CD8\u2009+\u2009cDNA microarrays of sorted T cells. Comparing the expression of Co-IRs on T cells and serum soluble mediators among healthy and SLE phenotypes.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>SLE patients with ESRD were downregulated CD38, PLEK, interferon-\u03b3, CX3CR1, FGFBP2, and SLCO4C1 transcripts on CD4\u2009+\u2009and CD8\u2009+\u2009T cells simultaneously and NKG7, FCRL6, GZMB\/H, Fc\u03b3RIII, ITGAM, Fas ligand, TBX21, LYN, granulysin, CCL4L1, CMKLR1, HLA-DR\u03b2, KIR2DL3, and KLRD1 in CD8 T cells. Pathway enrichment and PPI network analyses revealed that the overwhelming majority of Differentially Expressed Genes (DEGs) have been affiliated with novel cytotoxic, antigen presentation, and chemokine-cell migration signature pathways. CD8\u2009+\u2009GZMK\u2009+\u2009T cells that are varied in nature, including CD161\u2009+\u2009Mucosal-associated invariant T (MAIT) cells and CD161- aged-associated T (Taa) cells and CD161-GZMK\u2009+\u2009GZMB\u2009+\u2009T cells might account for a higher level of GZMK in CD8\u2009+\u2009T cells associated with ESRD. SLE patients have higher TIGIT\u2009+\u2009, PD1\u2009+\u2009, and lower CD127\u2009+\u2009cell percentages on CD4\u2009+\u2009T cells, higher TIM3\u2009+\u2009, TIGIT\u2009+\u2009, HLA-DR\u2009+\u2009cell frequency, and lower MFI expression of CD127, CD160 in CD8 T cells. Co-IRs expression in T cells was correlated with soluble PD-1, PDL-2, and TIM3 levels, as well as SLE disease activity, clinical phenotypes, and immune-therapy responses.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>The signature of dysfunctional pathways defines a distinct immunity pattern in LN ESRD patients. Expression levels of Co-IRs in peripheral blood T cells and serum levels of soluble PD1\/PDL-2\/TIM3 can serve as biomarkers for evaluating clinical parameters and therapeutic responses.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12929-024-01024-7","type":"journal-article","created":{"date-parts":[[2024,4,22]],"date-time":"2024-04-22T04:01:53Z","timestamp":1713758513000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["T cell expressions of aberrant gene signatures and Co-inhibitory receptors (Co-IRs) as predictors of renal damage and lupus disease activity"],"prefix":"10.1186","volume":"31","author":[{"given":"Chin-Man","family":"Wang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yeong-Jian","family":"Jan Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian-Wen","family":"Zheng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li Yu","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keng Poo","family":"Tan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5661-6291","authenticated-orcid":false,"given":"Ji-Yih","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,4,22]]},"reference":[{"key":"1024_CR1","doi-asserted-by":"publisher","first-page":"575","DOI":"10.1038\/cmi.2017.137","volume":"15","author":"P Zhang","year":"2018","unstructured":"Zhang P, Lu Q. 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