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FT500 as Monotherapy and in Combination With Immune Checkpoint Inhibitors in Subjects With Advanced Solid Tumors

ABSTRACT: FT500 is an off-the-shelf, iPSC-derived NK cell product that can bridge innate and adaptive immunity, and has the potential to overcome multiple mechanisms of immune checkpoint inhibitor (ICI) resistance. The preclinical data provide compelling evidence supporting the clinical investigation of FT500 as monotherapy and in combination with ICI in participants with advanced solid tumors.

DISEASE(S): Microsatellite Instability,Carcinoma,Small Cell Lung Cancer,Egfr Positive Solid Tumor,Advanced Solid Tumors,Colorectal Cancer,Urothelial Carcinoma,Head And Neck Neoplasms,Carcinoma, Merkel Cell,Neoplasms,Pancreas Cancer,Nsclc,Gastric Cancer,Advanced Solid Tumor,Squamous Cell Carcinoma,Colorectal Neoplasms,Her2-positive Breast Cancer,Renal Cell Carcinoma,Stomach Neoplasms,Pancreatic Neoplasms,Hepatocellular Carcinoma,Cervical Cancer,Melanoma,Small Cell Lung Carcinoma,Merkel Cell Carcinoma,Breast Cancer,Lymphoma,Carcinoma, Squamous Cell,Head And Neck Cancer

PROVIDER: 2297199 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Checkpoint Inhibitors Modulate Plasticity of Innate Lymphoid Cells in Peripheral Blood of Patients with Hepatocellular Carcinoma

Project description:Introduction: The role of innate lymphoid cells (ILC) in cancer and specifically in the context of hepatocellular carcinoma (HCC) is not well understood. Immune checkpoint inhibitors (ICI) have been approved for treatment of patients with HCC. The effect of ICI on ILCs has not been explored. Methods: We studied ILCs in PBMCs of 51 patients with HCC at baseline and after treatment with ICI. Flow cytometry was used to study ILC composition. Single-cell RNA-sequencing using a targeted panel of 405 immune-related genes was used to characterize the transcriptomic profiles as well as cellular trajectory of ILCs before and after ICI therapy. Intracellular cytokine staining was used to validate ILC function. Data from large patient cohorts were used to predict association with survival. Results: Characterization of the ILC subgroups in PBMCs of HCC patients revealed a significant increase in ILC1 and a decrease in ILC3 frequencies. Single cell RNA-sequencing identified a subgroup of NK-like ILCs which expressed cytotoxicity markers as well as NKp80/KLRF1. This KLRF1high-NK-like population showed low abundance in patients with HCC and was enhanced after combined anti-CTLA-4 and anti-PD-1 immunotherapy. Trajectory analysis placed this population in between ILC1 and ILC3s. The transcriptomic signature of KLRF1high NK-like ILCs was associated with better progression-free survival in HCC cohorts. Conclusions: We present a previously unknown effect of HCC tumors and ICIs on the composition and plasticity of ILCs in PBMCs. We identified a cytotoxic KLRF1high-NK-like subgroup which was associated with better survival, absent in untreated HCC patients, and enhanced upon ICI immunotherapy. Thus, ILCs from PBMC can be used to study changes in the innate immune system under immunotherapy.

2022-06-23 | GSE195648 | GEO

Regulation of iNKT cell development and function by METTL3

Project description:Invariant natural killer T (iNKT) cells are a specific innate-like counterpart of T lymphocytes, which response to lipid-based antigens and provide a functional bridge between the innate and adaptive immunity. The physiological role of m6A modification involved in NK cells differentiation remains unclear. We found that N6-Methyladenosine (m6A) methyltransferase METTL3 is intrinsically required for iNKT cell development and function in an m6A-dependent manner. To investigate the molecular mechanisms, RNA-seq was performed using iNKT cells in thymocytes isolated from WT and KO mice to investigate the regulatory network.

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m6A modification in DP and iNKT cells

Project description:Invariant natural killer T (iNKT) cells are a specific innate-like counterpart of T lymphocytes, which response to lipid-based antigens and provide a functional bridge between the innate and adaptive immunity. The physiological role of m6A modification involved in NK cells differentiation remains unclear. We found that N6-Methyladenosine (m6A) methyltransferase METTL3 is intrinsically required for iNKT cell development and function in an m6A-dependent manner. To investigate the molecular mechanisms, m6A-LACE-seq was performed using iNKT cells and Merip-seq was performed using DP cells in thymocytes isolated from WT and KO mice to investigate the regulatory network.

2023-12-31 | GSE210325 | GEO

Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection [scRNAseq_spleen_LN_total_NK]

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2021-08-25 | GSE180977 | GEO

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2021-08-25 | GSE180975 | GEO

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Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection [bulk_RNAseq_steady_state]

2021-08-25 | GSE180973 | GEO

Differential gene expression in human myeloid dendritic cells interacting with different knockout strains of Aspergillus fumigatus in vitro

Project description:Dendritic cells (DC) are the most important antigen presenting cells and play a pivotal role in host immunity to infectious agents by acting as a bridge between the innate and adaptive immune systems. Myeloid DCs (mDC) were isolated from peripheral blood and co-cultured with conidia (con) and germlings (ks) of Aspergillus fumigatus knockout (mitA, mnt1, rodA) and wildtype (wt) strains for 6 hours at an MOI of 1. RNA was extracted and hybridised to microarrays. Microarrays contain probes for approximately 110 selected human immune-relevant genes, including cytokine and chemokine genes, their receptors and downstream innate immunity genes. We used microarrays to detail the gene expression of human myeloid dendritic cells after 6h of co-cultivation with Aspergillus fumigatus wildtype and knockout mutants

2012-04-16 | E-GEOD-34884 | biostudies-arrayexpress

Faecalibaterium prausnitzii strain EXL01 boosts efficacy of Immune Checkpoint Inhibitors

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