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A Study to Explore the Third-line Treatment of Fruquintinib Combined With Serplulimab in Advanced Non-isolated Hepatic Metastatic Colorectal Cancer: a Single-center, Phase 2 Study

ABSTRACT: The aim of this clinical trial is to learn about efficacy of fruquintinib combined with serplulimab in patients with microsatellite stabilized mCRC who have failed standard therapy. The main purpose is to explore efficacy, safety and tolerability of the treatment. At the same time, the correlation between biomarkers (including ctDNA, TPS, CPS, tumor mutation burden, lymphocyte subpopulation, cytokines, TCR, intestinal microbes, etc.) and the efficacy and drug resistance mechanism will be analyzed, which could provide reference for determining the advantaged group.

DISEASE(S): Colorectal Cancer,Colorectal Neoplasms

PROVIDER: 67167 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Vitamin E Combined With Fruquintinib and Tislelizumab in Microsatellite Stabilized Metastatic Colorectal Cancer Patients

Project description:The goal of this clinical trial is to learn about efficacy of Vitamin E in combination with Fuquinitinib and Tirelizumab in patients with microsatellite stabilized mCRC who have failed standard therapy. The main question is to explore the survival time, safety and tolerability of the treatment. At the same time, the correlation between biomarkers (including PD-L1 expression, tumor mutation load, lymphocyte subpopulation, cytokines, TCR, intestinal microbes, and others) and the efficacy and drug resistance mechanism will be analyzed, so as to provide reference for the subsequent guidance of the screening of benefit groups.

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The resting and ligand-bound states of the membrane-embedded human T-cell receptor–CD3 complex

Project description:The T-cell receptor (TCR) initiates T-lymphocyte activation, but the mechanism of TCR activation remains uncertain. Here, we present cryogenic electron microscopy structures for the unliganded and human leukocyte antigen (HLA)-bound human TCR–CD3 complex in nanodiscs that provide a native-like lipid environment. Distinct from the “open and extended” conformation seen in detergent, the unliganded TCR–CD3 in nanodiscs adopts two related “closed and compacted” conformations that represent its physiologic resting state in vivo. By contrast, the HLA-bound complex adopts the open and extended conformation, and conformation-locking disulfide mutants show that ectodomain opening is necessary for maximal ligand-dependent T-cell activation. These structures also reveal conformation-dependent protein–lipid and glycan–glycan interactions within the TCR. Together, these results establish allosteric conformational change during TCR activation, reveal avenues for immunotherapeutic engineering, and highlight the importance of native- like lipid environments for membrane protein structure determination.

2025-12-17 | PXD070648 | Pride

UV-specific and -indepent interactors

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TCR-seq of each iNKT subset isolated from the thymus of BALB/c and B6 mice

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Integrative responses to IL-17 and TNF-α in human keratinocytes account for key inflammatory pathogenic circuits in psoriasis

Project description:We sought to provide a comprehensive evaluation of the effects of TNF-α and IL-17 on the keratinocyte gene profile in order to identify genes that might be co-regulated by these cytokines. We then sought to determine how genes that were synergistically activated by both cytokines relate to the psoriasis transcriptome. Here, we identified 160 unique genes that were synergistically up-regulated by IL-17 and TNF-α and 188 unique genes where the two cytokines had at least an additive effect. Among highly up-regulated genes were those involved in neutrophil and lymphocyte chemotaxis, inflammation, and epidermal differentiation. Synergistically up-regulated genes included some of the highest expressed genes in lesional psoriatic skin with an impressive correlation between IL-17/TNF-α induced genes and the psoriasis gene signature. In conclusion, keratinocytes may be key drivers of pathogenetic inflammatory circuits in psoriasis through integrating responses to TNF-α and IL-17. This may explain high efficacy of targeting psoriasis with either anti-TNF-α or agents that block Th17 T-cells/IL-17 and has important implications for the development of new therapeutic agents. Comparison of keratinocyte responses to IL-17, TNF-α (1 ng mL-1 and 10 ng mL-1), and the combination of both cytokines in psoriasis.

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2012-12-29 | E-GEOD-32315 | biostudies-arrayexpress

Single cell transcriptomic analysis (10x Genomics) of mouse colon LP CD4+ Tcells cells isolated from mouse under different infection conditions [bulk RNA]

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