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Transcriptional responses of T cells activated via CD22-specific T cell receptor compared to CD22-specific chimeric antigen receptor

ABSTRACT: Transcriptional responses of T cells activated via CD22-specific T cell receptor compared to CD22-specific chimeric antigen receptor

PROVIDER: PRJNA1074674 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27911621_1.fastq.gz	Fastqsanger.gz
	SRR27911621_2.fastq.gz	Fastqsanger.gz
	SRR27911622_1.fastq.gz	Fastqsanger.gz
	SRR27911622_2.fastq.gz	Fastqsanger.gz
	SRR27911623_1.fastq.gz	Fastqsanger.gz

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Transcriptional responses of T cells activated via CD22-specific T cell receptor compared to CD22-specific chimeric antigen receptor

Project description:Chimeric antigen receptor (CAR) T cells are effective against B-cell malignancies but are associated with cytokine-driven inflammatory toxicities such as cytokine release syndrome (CRS). Historically, T cell receptor (TCR) engineered T cell therapies are rarely associated with CRS. However, it is challenging to compare diverse cell products utilized in different clinical contexts and against different antigens. In this study, TCR and CAR were made to target the same source of antigen, CD22, expressed by B-cell malignancies: the TCR recognizes CD22-derived peptide processed and presented in the context of HLA-A*02:01, and the CAR recognizes CD22 protein expressed on the cell surface. In vivo studies comparing the CD22 TCR-T cells to CD22 CAR-T cells demonstrated that the TCR-T cells could clear leukemia without inducing systemic proinflammatory cytokine elevation, whereas CD22 CAR-T cells induced high levels of circulating proinflammatory cytokine reminiscent of CRS. T cells activated through either the TCR or CAR by an identical leukemia cell line demonstrated differential transcriptional responses. T cells activated via the CAR had disproportionate and significant upregulation of inflammatory gene sets compared to T-cells activated via the TCR.

2025-04-16 | GSE255323 | GEO

CD22 interactome

Project description:CD22 (Siglec-2) is a member of the Siglec family. It is an inhibitory co-receptor of the B-cell-receptor (BCR) and inhibits B–cell activation. Upon BCR stimulation ITIMs in the cytoplasmic tail of CD22 are phosphorylated. This triggers CD22 signalling pathways, which lead to a decreased calcium mobilization in the B cell and thus an inhibition of BCR signalling. Although some CD22 binding partners, such as the phosphatase SHP-1, have already been identified, we deciphered the CD22 interactome in more detail, to gain a deeper understanding of CD22 molecular mechanisms and signalling events after BCR activation. Stable isotope labelling of amino acids in cell culture (SILAC) in combination with mass spectrometry analysis enabled the identification of specific CD22 interaction partners in a quantitative proteomics approach. Hereby, several new CD22 associated proteins were identified that have not been linked to CD22 yet. One of those interacting proteins is cullin 3, an E3 ubiquitin ligase. It was revealed that cullin 3 is important for clathrin-dependent CD22 internalization after BCR stimulation and CD22 surface expression. Further analysis of B-cell specific cullin 3 deficient mice showed an important role of cullin 3 in B cell development. These mice have strongly reduced numbers of mature B cells in the periphery, which are characterized by increased CD22 expression and additionally by pre-activated and apoptotic phenotypes.

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chimeric antigen receptor T cells with knockout

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Project description:This clinical trial is an open-label, single-centre, dose escalation, phase I study designed to investigate the safety and tolerability of Haploidentical / Allogeneic NKG2DL-targeting Chimeric Antigen Receptor-grafted Gamma Delta (γδ) T Cells (CTM-N2D) in Subjects with Relapsed or Refractory Solid Tumour. The study objectives of this phase I study are to determine the safety, activity and the safe dose of haploidentical or allogeneic NKG2DL-targeting chimeric antigen receptor-grafted γδ T cells given four times weekly in patients with relapsed or refractory solid tumors of different types.

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Project description:In this data set we include expression data from human CD4+ T cells isolated on day 0, 6, 11 and 24 follow anti-CD3/anti-CD28 magnetic bead stimulation and chimeric antigen receptor transduction. 30 samples were submitted. Samples represented three biological replicates of normal donors transduced with various CARs. CARs used were a cMet 28z specific CAR comprised of the IgG4 hinge, CD28 transmembrane and CD28 and CD3zeta intracellular domains. A CD19 CD28 CAR was specific to CD19, and was comprised of a CD8a hinge, CD28 transmembrane and CD28 and CD3zeta intracellular domain. A third CAR, the CD19 BBz, was used that was specific to CD19 was comprised of a CD8a hinge, CD8a transmembrane and 4-1BB and CD3zeta intracellular domains. Expression data was analyzied on day 0, 6, 11 and 24.

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Project description:Chimeric antigen receptor (CAR) T-cell therapy has had considerable success in the treatment of B-cell malignancies. Targeting the B-lineage marker CD19 has brought great advances to the treatment of acute lymphoblastic leukemia and B-cell lymphomas. However, relapse remains an issue in many cases. Such relapse can result from downregulation or loss of CD19 from the malignant cell population or expression of alternate isoforms. Consequently, there remains a need to target alternative B-cell antigens and diversify the spectrum of epitopes targeted within the same antigen. CD22 has been identified as a substitute target in cases of CD19-negative relapse. One anti-CD22 antibody-clone m971-targets a membrane-proximal epitope of CD22 and has been widely validated and used in the clinic. Here, we have compared m971-CAR with a novel CAR derived from IS7, an antibody that targets a central epitope on CD22. The IS7-CAR has superior avidity and is active and specific against CD22-positive targets, including B-acute lymphoblastic leukemia patient-derived xenograft samples. Side-by-side comparisons indicated that while IS7-CAR killed less rapidly than m971-CAR in vitro, it remains efficient in controlling lymphoma xenograft models in vivo. Thus, IS7-CAR presents a potential alternative candidate for the treatment of refractory B-cell malignancies.

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Identification of transcription factors regulating CD22 transcription

Project description:CD22 (also known as Siglec-2) belongs to the Siglec family of glycan-recognition proteins and negatively regulates B-cell receptor-mediated signaling. CD22 protein is known to be down-regulated in the B cells of patients with chronic lymphocytic leukemia (CLL). However, the mechanism regulating the transcription of CD22 is incompletely understood. In this study, we defined the minimal promoter region of the human CD22 gene, and systematically identified the proteins binding to the minimal promoter by DNA affinity-purification from the nuclear extracts of B cell lines and LC-MS/MS.

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Project description:The molecules of programmed cell death protein-1 (PD-1) and ligand-1 (PD-L1) become new therapeutic targets for cancer therapy. Although tumor-expressed PD-L1 molecule is frequently dispensable for checkpoint blockade in some cancer patients, recent studies suggest that T cell-expressed PD-L1 molecule might play a crucial role in antitumor immunity. Here, to investigate CD22 chimeric antigen receptor (CAR)-T cell therapy, we have generated the different CD22 CAR-T constructs. We noticed that tumor cells induced PD-L1 expression on the surface of CD22 CAR-T cells. The induced PD-L1 might limit immunogenic responses of CAR-T cells. T cell-expressed PD-L1 leads to a suppressive signal by PD-1/PD-L1 engagement of CD22 CAR-T cells. Meanwhile, PD-L1 suppresses CD22 CAR-T cell differentiation into memory T cells and negatively affected secretions of several essential cytokines, such as interleukin-2 (IL-2) and tumor necrosis factor (TNF)-α. We further observed that anti-PD-L1 monoclonal antibodies rescued cytokine secretion of CD22 CAR-T cells rather than anti-PD-1 monoclonal antibodies. Our current studies provide a potential mechanism to understand the functions and roles of T cell-expressed PD-L1 in tumor microenvironment. These results will encourage the physicians to re-recognize the important roles of PD-L1 in cancer immunotherapy studies and provide the helpful guidance for clinical operation of PD-L1 inhibition drugs.

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