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Disruption of Fibroblast MYD88 Signaling Promotes Antitumor Immunity in Pancreatic Ductal Adenocarcinoma [scRNAseq_ICBCA4948tx]

ABSTRACT: Disruption of Fibroblast MYD88 Signaling Promotes Antitumor Immunity in Pancreatic Ductal Adenocarcinoma [scRNAseq_ICBCA4948tx]

PROVIDER: PRJNA1222859 | ENA |

REPOSITORIES: ENA

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Disruption of Fibroblast MYD88 Signaling Promotes Antitumor Immunity in Pancreatic Ductal Adenocarcinoma [scRNAseq_col1a1myd88]

Project description:Disruption of Fibroblast MYD88 Signaling Promotes Antitumor Immunity in Pancreatic Ductal Adenocarcinoma [scRNAseq_col1a1myd88]

| PRJNA1222855 | ENA

Disruption of Fibroblast MYD88 Signaling Promotes Antitumor Immunity in Pancreatic Ductal Adenocarcinoma [scRNAseq_col1a1myd88]

Project description:Pancreatic ductal adenocarcinoma (PDAC) continues to carry a dismal prognosis. The disease is characterized by a uniquely dense fibrotic matrix generated by cancer-associated fibroblasts (CAFs). We have previously demonstrated that fibroblast-driven chronic inflammation suppresses T cell function through a MYD88-dependent mechanism. While extensively studied in myeloid cells, the role of MYD88 signaling in CAFs and its effects on PDAC remain poorly understood. In this study, we identify a MYD88-driven inflammatory CAF population in PDAC using a combination of bulk, single-cell, and spatial transcriptomic studies. Using an innovative collagen gel implantation model, we demonstrate that loss of MYD88 in CAFs enhances T cell infiltration and suppresses tumor growth. Combining MYD88 inhibition with immune checkpoint blockade significantly reduces tumor size and enhances antitumor immune responses, underscoring its potential as a therapeutic target in PDAC.

2025-08-19 | GSE289400 | GEO

Disruption of Fibroblast MYD88 Signaling Promotes Antitumor Immunity in Pancreatic Ductal Adenocarcinoma [scRNAseq_ICBCA4948tx]

2025-08-19 | GSE289401 | GEO

Disruption of Fibroblast MYD88 Signaling Promotes Antitumor Immunity in Pancreatic Ductal Adenocarcinoma [BulkRNA-seq_LPSstim]

2025-08-19 | GSE289399 | GEO

Disruption of Fibroblast MYD88 Signaling Promotes Antitumor Immunity in Pancreatic Ductal Adenocarcinoma [BulkRNA-seq_LPSstim]

Project description:Disruption of Fibroblast MYD88 Signaling Promotes Antitumor Immunity in Pancreatic Ductal Adenocarcinoma [BulkRNA-seq_LPSstim]

| PRJNA1222852 | ENA

MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut III

Project description:Fibroblasts that reside in the gut mucosa are among the key regulators of innate immune cells, but their role in the regulation of the defense functions of macrophages remains unknown. MyD88 is suggested to shape fibroblast responses in the intestinal microenvironment. We found that mice lacking MyD88 in fibroblasts showed a decrease in the colonic antimicrobial defense, developing dysbiosis and aggravated DSS-induced colitis. These pathological changes were associated with accumulation of Arginase 1+ macrophages with low antimicrobial defense capability. Mechanistically, production of IL-6 and CCL2 downstream of MyD88 was critically involved in fibroblast-mediated support of macrophage antimicrobial function, and IL-6/CCL2 neutralization resulted in the generation of macrophages with decreased production of antimicrobial peptide cathelicidin and impaired bacterial clearance. Collectively, these findings revealed a critical role of fibroblast-intrinsic MyD88 signaling in regulating macrophage antimicrobial defense under colonic homeostasis, and its disruption results in dysbiosis, predisposing host to the development of intestinal inflammation.

2025-03-05 | GSE291182 | GEO

MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut II

2025-03-05 | GSE291180 | GEO

MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut IV

2025-03-05 | GSE291184 | GEO

MyD88-mediated signaling in intestinal fibroblasts regulates macrophage antimicrobial defense and prevents dysbiosis in the gut I

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Chimeric Antigen Receptors with a MyD88 and CD40 costimulatory endodomain endow T cells with superior antitumor activity

Project description:CAR T-cell therapy for solid tumors has shown limited efficacy in early phase clinical studies. The majority of CARs encode CD28 and/or 41BB costimulatory endodomains and we explored here if MyD88 and CD40 (MC) costimulatory endodomains in CARs improve their antitumor activity. We generated CD28-, 41BB-, and MC-CAR T-cells and demonstrate that MC-CAR T-cells have greater proliferative capacity and antitumor activity in repeat stimulation assays and in tumor models in vivo. Transcriptomic analysis revealed that MC-CAR T-cells expressed higher levels of MYB and FOXM1, key cell cycle regulators, and are activated at base line. After stimulation, MC-CAR T-cells remain in a less differentiated state than CD28- and 41BB-CAR T-cells as judged by low levels of TBET and BLIMP1 expression, and lower cytolytic activity in comparison to CD28- and 41BB-CAR T-cells. Thus, including MyD88 and CD40 signaling domains in CARs may improve current CAR T-cell therapy approaches for solid tumors.

2020-09-18 | GSE158144 | GEO

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