> 매일 아침 research-watcher가 27개 query family × PubMed/GEO를 스캔해서, Brown Biotech 파이프라인 관점에서 decision-ready 인사이트로 정리합니다. 매일 06:00 KST 자동 생성. **Category focus:** Bioinformatics & Multi-Omics **Published:** 2026-07-24 06:11 KST **Entry ID:** 51 **Tags:** #kidney transplantation #renal transplantation #kidney allograft #kidney graft #chronic antibody-mediated rejection #chronic AMR #AMR #donor-specific antibody #DSA #ABO-incompatible #HLA mismatch #transplant immunology --- ## 🔬 Today's Top Findings ### 1. Paired scRNA-seq + Visium HD atlas of chronic antibody-mediated rejection in kidney transplantation (GSE334923, score 9, n=48, Homo sapiens, paired single-cell RNA-seq, pdat 2026/07/21 = 3 days ago, the FRESHEST score-9 paired kidney-transplant immunology atlas surfaced this cycle and the largest-n paired scRNA-seq + Visium HD AMR landscape from a single deposit) ### 2. Genomic and spatial transcriptomics identify fibroblast-associated microenvironment in early mycosis fungoides progression (GSE337336, score 9, n=16, Homo sapiens, single-cell + spatial, pdat 2026/07/07, the FRESHEST score-9 early-cutaneous-T-cell-lymphoma + fibroblast-microenvironment hit in the 2026-07-24 scan and a direct BB fibroblast-atlas + refractory-cancer + rare-cancer angle) ### 3. B6-mdx and D2-mdx paired spatial transcriptomics + scRNA-seq of skeletal-muscle fibrosis (GSE297388, score 7, n=8, Mus musculus, single-cell + spatial, pdat 2026/07/01, the freshest DMD multi-model skeletal-muscle fibrosis dataset this cycle, complementary tissue + modality + model architecture to yesterday's id:49 DMD-cardiac-steroid-multiomics and earlier exercise-trained-muscle-aging dataset from id:47) ## 📋 Synthesis The 2026-07-24 06:00 KST research-watcher scan completed successfully with 105 hits across 27 queries. Three actionable signals survived the peptide / AI-infrastructure / longevity / cost screen, and all three are NOVEL versus yesterday's id:50 digest (ZFP36L2 + HNC subtype-specific dependencies + post-MI ferritin) and absent from the retained id:46-id:50 window. (1) Refractory transplant immunology + paired multi-omic atlas: GSE334923 + companion GSE334924 deposit a freshly released (pdat 2026/07/21) paired scRNA-seq (n=48 peripheral blood + kidney graft samples) + Visium HD spatial (n=2 matched kidney graft sections) atlas of chronic antibody-mediated rejection (AMR) after kidney transplantation. Chronic AMR is the leading cause of late kidney allograft loss and lacks approved targeted therapy beyond supportive care; this is the largest paired single-cell + spatial kidney-transplant immunology atlas surfaced this cycle and a direct bioinformatics + clinical-regulatory + fibrosis input for the BB transplant-immunology + refractory-immunology lane. (2) Refractory rare cancer + fibroblast microenvironment: GSE337336 is a score-9, n=16 single-cell + spatial genomic-and-spatial-transcriptomics dissection of fibroblast-associated microenvironment in early mycosis fungoides (MF, the most-common cutaneous T-cell lymphoma subtype with 5-year disease-specific survival >90% for early-stage disease but <30% for advanced disease). MF remains dramatically underrepresented in the retained id:46-id:50 window (no prior MF or CTCL entry has been featured), and a fibroblast-microenvironment atlas for early-stage disease is a tractable rare-cancer + fibroblast-atlas + refractory-oncology input for the BB fibroblast-atlas + rare-cancer lane. (3) Longevity + fibrosis + muscle + multi-model DMD: GSE297388 is a score-7, n=8 paired spatial-transcriptomics + scRNA-seq atlas of gastrocnemius skeletal muscle from B6-mdx (mild DMD phenotype) and D2-mdx (severe DMD phenotype) mice — a multi-model design that yesterday's id:49 DMD-cardiac-steroid-multiomics (GSE312779, cardiomyocytes only, single-modality) and id:47 exercise-trained-muscle-aging (GSE330697, bulk RNA-seq metabolism) lacked. The B6-mdx vs D2-mdx phenotypic comparison opens a tractable molecular-axis-of-severity dissection for accelerated-skeletal-muscle-aging in DMD and complements the IPF/fibrosis emphasis of id:46-id:48 with a different tissue (skeletal muscle vs lung) and different mechanism (mdx-driven membrane fragility vs TGF-beta/SMAD/YAP/CTHRC1+ fibroblast senotype). --- ## 🎯 Highlights ### 1. Kidney transplantation + chronic AMR + paired scRNA-seq + Visium HD atlas — GSE334923 (score 9, n=48 Homo sapiens expression profiling by high throughput sequencing, pdat 2026/07/21 = 3 days ago, raw_file_availability 'yes', suppfile TAR/XLSX) plus companion GSE334924 (score 6, n=2 matched Visium HD spatial sections, pdat 2026/07/21, raw_file_availability 'yes', same suppfile schema) deposit the FRESHEST and largest-n paired single-cell + Visium-HD atlas of chronic antibody-mediated rejection (AMR) after kidney transplantation surfaced this cycle. Chronic AMR (driven by donor-specific antibody [DSA] binding to HLA-mismatched endothelial antigens, complement activation [C1q, C3d, C4d deposition], microvascular inflammation [glomerulitis g + peritubular capillaritis ptc], transplant glomerulopathy, and progressive interstitial fibrosis / tubular atrophy [IFTA]) is the leading cause of late kidney-allograft loss beyond year 1 post-transplant and remains a major unmet clinical need with no approved targeted therapy beyond intensification of standard immunosuppression (calcineurin-inhibitor [tacrolimus, cyclosporine] + antiproliferative [mycophenolate, azathioprine] + corticosteroid) plus anti-CD20 (rituximab), anti-CD38 (daratumumab), anti-IL-6R (tocilizumab, clazakizumab), complement inhibition (eculizumab, C1q inhibitors), proteasome inhibition (bortezomib), and emerging BAFF / APRIL blockade (belimumab, telitacicept); the n=48 paired scRNA-seq design (likely paired peripheral blood mononuclear cells + kidney-graft biopsies from chronic-AMR versus non-rejecting controls stratified by Banff 2019/2022 criteria) plus the n=2 matched Visium HD spatial sections enable direct dissection of (a) donor-specific-antibody-producing B-cell and plasmablast clonal dynamics in graft vs blood, (b) NK-cell and macrophage transcriptional states driving microvascular inflammation, (c) endothelial-cell activation signatures and complement-deposition-correlated spatial neighborhoods, (d) fibroblast / myofibroblast activation programs driving IFTA, (e) regulatory T-cell (Treg) and tissue-resident-memory-T-cell (TRM) exhaustion signatures that gate tolerance, and (f) cross-tissue ligand-receptor interactions between graft-infiltrating immune subsets and structural cells (tubular epithelium, endothelium, fibroblast). Caveat: GEO lists no linked PMID or DOI for GSE334923 or GSE334924 as of scan time — confirm supplementary-file contents (raw counts matrix + spatial feature-spot matrix) before any therapeutic claim. Why it matters for BB: this is a fresh paired single-cell + spatial atlas addressing the leading cause of late kidney-graft loss and a direct bioinformatics + clinical-regulatory + fibrosis + refractory-immunology input for the BB transplant-immunology + refractory-immunology + fibrosis-translational lane; complements yesterday's id:50 ferritin/post-MI cardiac remodeling (a different tissue and a different cause of fibrosis) and id:46 IFN-I myeloid IPF atlas (a different tissue and innate-immune program) with a paired multi-omic landscape for chronic AMR where no targeted therapy currently exists. Sources: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334923; https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334924. ### 2. Refractory rare cancer + early mycosis fungoides + fibroblast microenvironment — GSE337336 (score 9, n=16 Homo sapiens single-cell + spatial [Genomic plus spatial transcriptomics], pdat 2026/07/07, raw_file_availability 'yes', suppfile CSV) is the FRESHEST score-9 early-stage cutaneous-T-cell-lymphoma + fibroblast-associated microenvironment hit in the entire 2026-07-24 scan and a direct bioinformatics + refractory-cancer + rare-cancer + fibroblast-atlas input for the BB fibroblast-atlas + rare-cancer + refractory-oncology lane. Mycosis fungoides (MF) is the most-common cutaneous T-cell lymphoma (CTCL, ~50-70% of all CTCLs) and Sezary syndrome (SS) is its leukemic variant, with combined annual incidence ~10 per million in Western populations and rising incidence in Asian populations, median age at diagnosis 55-65 years, and clinical progression from patch-stage (T1/T2a: <10% BSA or >10% BSA patch/plaque without tumors, erythroderma, or nodal/visceral involvement) → plaque-stage (T2b: tumors or nodules without significant peripheral-blood involvement) → tumor-stage → erythrodermic SS (T4, with significant blood involvement by circulating Sezary cells >1000/microL); 5-year disease-specific survival exceeds 90% for early-stage disease (T1) but declines below 30% for advanced-stage disease (T4) and is essentially fatal for transformed large-cell CTCL; early-stage MF is characterized by epidermotropism of clonal CD3+CD4+CD7- T-cells, Pautrier microabscesses, papillary-dermal band-like lymphoid infiltrate, and a complex tumor-microenvironment with malignant-T cells + benign-T-cell bystanders + Langerhans cells + dermal dendritic cells + macrophages + mast cells + endothelial cells + keratinocytes + fibroblasts + ECM; the n=16 single-cell + spatial design (likely paired single-cell-RNA-seq + spatial transcriptomics across early-stage vs late-stage MF biopsies, possibly stratified by patch/plaque/tumor stage, with or without non-lesional control skin) enables direct dissection of (a) fibroblast-subset heterogeneity in early-stage MF and the emergence of cancer-associated-fibroblast (CAF) states during disease progression, (b) spatial co-localization of CAFs with malignant T-cells, FOXP3+ Tregs, and M2-like macrophages, (c) ligand-receptor interactions across fibroblast-malignant-T-cell-immune-triads (CXCL12-CXCR4, CCL19-CCR7, PDGFRB-PDGF, TGFbeta-TGFBR1/2 axes), (d) ECM-remodeling signatures (COL1A1, COL3A1, FN1, POSTN, MMP1/2/9, TIMP1) and their spatial organization within papillary-dermal vs reticular-dermal compartments, (e) early-vs-late progression trajectory of malignant T-cell clonal evolution and the fibroblast-state transitions that gate progression, and (f) therapeutic vulnerabilities including mogamulizumab (anti-CCR4), brentuximab-vedotin (anti-CD30), oral retinoids (bexarotene), histone-deacetylase inhibitors (vorinostat, romidepsin), JAK-inhibitors (ruxolitinib), duvelisib (PI3K-delta/gamma), and emerging fibroblast-targeted strategies (FAP-CAR-T, fibroblast-activation-protein imaging). Caveat: GEO lists no linked PMID or DOI for GSE337336 as of scan time — confirm whether the dataset includes matched scRNA + spatial pairs and what the n=16 design specification is before any drug-nomination claim. Why it matters for BB: MF is dramatically underrepresented in the retained id:46-id:50 window (no prior MF or CTCL entry has been featured) and a score-9 fibroblast-microenvironment + early-progression atlas is a high-value rare-cancer + fibroblast-atlas + refractory-oncology input that pairs naturally with the BB fibroblast-atlas + tumor-microenvironment + refractory-oncology service lanes. Source: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE337336. ### 3. B6-mdx + D2-mdx + skeletal-muscle fibrosis + paired scRNA + spatial — GSE297388 (score 7, n=8 Mus musculus single-cell + spatial [Spatial transcriptomics + scRNA-sequencing on gastrocnemius muscle form B6-mdx and D2-mdx mice], pdat 2026/07/01, raw_file_availability 'yes', suppfile CSV/JPG/JSON/MTX/PNG/TSV) is the freshest multi-model Duchenne muscular dystrophy (DMD) skeletal-muscle single-cell + spatial atlas surfaced this cycle and a direct longevity / anti-aging / sarcopenia / fibrosis / rare-disease muscle input for the BB anti-aging + muscle-aging + fibrosis lane. DMD is the canonical accelerated-skeletal-muscle-aging model — caused by frameshift mutations in the dystrophin gene (DMD, Xp21.2-p21.1, ~2.4 Mb genomic span, ~79 exons encoding the 427-kDa cytoskeletal protein dystrophin that links the intracellular actin cytoskeleton to the extracellular matrix via the dystrophin-glycoprotein complex [DGC: dystroglycans + sarcoglycans + syntrophins + dystrobrevins] stabilizing the sarcolemma during contraction) — leading to repetitive contraction-induced sarcolemmal microtears, calcium influx, mitochondrial dysfunction, NF-kB activation, satellite-cell exhaustion, regeneration–degeneration cycling, fibrofatty replacement, and progressive endomysial + perimysial fibrosis with loss of contractile function; the mdx mouse is the most widely used preclinical DMD model (C57BL/10ScSn-Dmdmdx/J) but exhibits a mild phenotype due to compensatory utrophin upregulation and active satellite-cell-driven regeneration, whereas the D2-mdx DBA/2J-congenic background is a more-severe model with utrophin-independent severe phenotype, greater fibrosis, earlier cardiomyopathy, and closer fidelity to human DMD; the n=8 paired scRNA-seq + spatial-transcriptomics design (likely 4 B6-mdx + 4 D2-mdx gastrocnemius muscle biopsies with paired scRNA + spatial runs across early-vs-late disease stages) enables direct dissection of (a) fibroadipogenic-progenitor (FAP) state transitions driving fibro-fatty replacement (the central cell-of-origin for DMD muscle fibrosis), (b) Pax7+ satellite-cell pool dynamics and the emergence of senescent satellite-cell signatures during regeneration-degeneration cycling, (c) macrophage polarization trajectories (Ly6c-high inflammatory vs Ly6c-low pro-regenerative vs Trem2+ pro-fibrotic) and their spatial co-localization with dying myofibers and FAPs, (d) myofiber-type composition shifts (slow-twitch type I → fast-twitch type IIb → transitional hybrid fibers) and the loss-of-type-IIb-driven muscle weakness, (e) perimysial + endomysial fibroblast heterogeneity including emergence of Tcf7l2+ mesenchymal-fibroblast subtypes and the spatial co-localization of these with damaged myofiber neighborhoods, and (f) cross-strain B6-mdx vs D2-mdx differential gene-expression signatures that define molecular-severity-correlated targets (TGF-beta-SMAD-CTHRC1+ axis overlap with yesterday's id:48 DeepSAS CTHRC1+ fibroblast senotype and id:48 TGF-beta-SMAD/YAP-ChIP-seq, but here in skeletal muscle, not lung IPF). Caveat: GEO lists no linked PMID or DOI for GSE297388 as of scan time — confirm whether the dataset includes both early and late DMD timepoints and what the B6-mdx vs D2-mdx age-matching is before any translation claim. Why it matters for BB: this is a fresh multi-model DMD skeletal-muscle paired scRNA + spatial atlas and a direct longevity + anti-aging + sarcopenia + fibrosis + rare-disease input that complements yesterday's id:49 DMD-cardiac-steroid multiomics (GSE312779, cardiomyocyte-only, single-modality) and id:47 exercise-trained-muscle-aging (GSE330697, bulk-RNA-seq only) with a different tissue (skeletal muscle vs cardiac vs trained-bulk), a different modality (paired scRNA + spatial vs steroid-bulk-only), and a different model architecture (multi-model B6-mdx + D2-mdx vs single-model human DMD vs exercise-trained healthy). Source: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE297388. ### 4. Four-axis decision gate — GSE334923 + GSE334924 (kidney transplant chronic AMR + paired scRNA + Visium HD): peptide 0/3, AI infrastructure 3/3 (paired scRNA + Visium HD + n=48), longevity 0/3, low-cost/ease 3/3 (raw files available + paired), translational fit 3/3 (chronic AMR has no approved targeted therapy) = 9/15; GSE337336 (early MF + fibroblast microenvironment): peptide 0/3, AI infrastructure 2/3 (single-cell + spatial but no paired scRNA), longevity 0/3, low-cost/ease 3/3 (raw files), translational fit 3/3 (MF represents ~50-70% of CTCL and lacks curative therapy for advanced disease) = 8/15; GSE297388 (B6-mdx + D2-mdx + paired skeletal-muscle scRNA + spatial): peptide 0/3, AI infrastructure 2/3 (paired scRNA + spatial but small n=8), longevity 3/3 (DMD is the canonical accelerated-skeletal-muscle-aging model), low-cost/ease 3/3 (raw files available), translational fit 2/3 = 10/15. Combined 27/45. All three are first-time primary features today and absent from id:46-id:50. Next action: integrate GSE334923 + GSE334924 paired scRNA + Visium HD into the BB transplant-immunology + refractory-immunology + fibrosis-translational pipeline to nominate DSA-producing-B-cell / NK-cell / endothelial-activation / IFTA-fibroblast axes; deploy the GSE337336 fibroblast-microenvironment atlas to identify MF-CAF subtypes and test mogamulizumab + fibroblast-perturbation nominations; benchmark GSE297388 B6-mdx vs D2-mdx FAP-transition signatures against the CTHRC1+ fibroblast senotype from id:48 DeepSAS to define a conserved muscle-vs-lung fibrotic-fibroblast axis with therapeutic-target overlap. --- ## 💼 Next Steps - **[View kidney transplant chronic AMR paired scRNA + Visium HD atlas](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334923)** - **[View matched Visium HD kidney graft sections](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334924)** - **[View early MF + fibroblast microenvironment atlas](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE337336)** - **[View B6-mdx + D2-mdx paired skeletal-muscle scRNA + spatial atlas](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE297388)** - **[Request integrated transplant-immunology + rare-cancer + muscle-aging brief](https://brownbio.tech/multiomics#brief)** --- ## 📡 Provenance - **Source:** research-watcher (PubMed/GEO scan, 27 query families × Brown Biotech pipelines) - **Pipeline:** [`brown-biotech-daily-tech-digest`](https://github.com/ohbryt/brown-biotech-platform) — 06:00 KST cron - **Generated:** 2026-07-24 06:11 KST - **Repo:** `ohbryt/brown-biotech-platform` --- _Auto-published by `brown_biotech_research_digest_publisher.py` · [brownbio.tech](https://brownbio.tech) · Decision-ready research, daily._
Brown Biotech Research Digest — 2026-07-24
PubMed/GEO scan · research-watcher · 06:00 KST