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Brain antigens stimulate proliferation of T lymphocytes with a pathogenic phenotype in multiple sclerosis patients

ABSTRACT: Brain antigens stimulate proliferation of T lymphocytes with a pathogenic phenotype in multiple sclerosis patients

PROVIDER: PRJNA795499 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17490300_1.fastq.gz	Fastqsanger.gz
	SRR17490300_2.fastq.gz	Fastqsanger.gz
	SRR17490301_1.fastq.gz	Fastqsanger.gz
	SRR17490301_2.fastq.gz	Fastqsanger.gz
	SRR17490302_1.fastq.gz	Fastqsanger.gz

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Brain antigens stimulate proliferation of T lymphocytes with a pathogenic phenotype in multiple sclerosis patients

Project description:A method to stimulate T lymphocytes with a broad range of brain antigens would facilitate identification of the autoantigens for multiple sclerosis and enable definition of the pathogenic mechanisms important for multiple sclerosis. In previous work we found the obvious approach of culturing leukocytes with homogenized brain tissue does not work because the brain homogenate suppresses antigen-specific lymphocyte proliferation. We now report a method that substantially reduces the suppressive activity. We used this non-suppressive brain homogenate to stimulate leukocytes from multiple sclerosis patients and controls. We also stimulated with common viruses for comparison. We measured proliferation, selected the responding CD3+ cells with flow cytometry, and sequenced their transcriptomes for mRNA and T cell receptor sequences. The mRNA expression suggested the brain-responding cells from MS patients are potentially pathogenic. The T cell receptor repertoire of the brain-responding cells was clonal with minimal overlap with virus antigens.

2022-01-13 | GSE193260 | GEO

Brain Antigens Stimulate Proliferation of T Lymphocytes With a Pathogenic Phenotype in Multiple Sclerosis Patients.

Project description:A method to stimulate T lymphocytes with a broad range of brain antigens would facilitate identification of the autoantigens for multiple sclerosis and enable definition of the pathogenic mechanisms important for multiple sclerosis. In a previous work, we found that the obvious approach of culturing leukocytes with homogenized brain tissue does not work because the brain homogenate suppresses antigen-specific lymphocyte proliferation. We now report a method that substantially reduces the suppressive activity. We used this non-suppressive brain homogenate to stimulate leukocytes from multiple sclerosis patients and controls. We also stimulated with common viruses for comparison. We measured proliferation, selected the responding CD3+ cells with flow cytometry, and sequenced their transcriptomes for mRNA and T-cell receptor sequences. The mRNA expression suggested that the brain-responding cells from MS patients are potentially pathogenic. The T-cell receptor repertoire of the brain-responding cells was clonal with minimal overlap with virus antigens.

| S-EPMC8841344 | biostudies-literature

Antigens expressed by breast cancer cells undergoing EMT stimulate cytotoxic CD8+ T cell immunity

Project description:Antigens expressed by breast cancer cells undergoing EMT stimulate cytotoxic CD8+ T cell immunity

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Siponimod selectively enriched regulatory T and B lymphocytes in active secondary progressive multiple sclerosis patients

Project description:Siponimod selectively enriched regulatory T and B lymphocytes in active secondary progressive multiple sclerosis patients: 20 SPMS baseline including 3 repeats, 19 treated with 5 placebo and 14 siponimod treated.

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Identification of target antigens of CSF OCB-derived monoclonal antibodies

Project description:The identification of target antigens recognized by monoclonal antibodies that have been derived from oligoclonal band IgG of CSF samples from multiple sclerosis patients.

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Antigens expressed by breast cancer cells undergoing EMT stimulate cytotoxic CD8+ T cell immunity

Project description:The transformation of carcinoma cells with epithelial characteristics to those with mesenchymal characteristics (termed EMT) facilitates the progression of localized breast cancer to metastatic disease. The EMT program also contributes to several immunosuppressive and immunoevasive properties, altering the susceptibility of the cells to immune cell recognition and killing. Therefore, the aim of our study was to identify antigens upregulated in the mesenchymal cell state and assess their ability to circumvent immune escape. We confirmed increased susceptibility to the killing of epithelial cells across all antigens tested.

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Nucleobase adducts bind MR1 and stimulate MR1-restricted T cells

Project description:MR1T cells are a recently discovered class of T cells that recognize antigens presented by the MHC-I–related molecule MR1 in the absence of microbial infection. The nature of the self-antigens that stimulate MR1T cells remains unclear, hampering our understanding of their physiological role and therapeutic potential. By combining genetic, pharmacological, and biochemical approaches, we found that carbonyl stress and changes in nucleobase metabolism in target cells promote MR1T cell activation. Stimulatory compounds formed by carbonyl adducts of nucleobases were detected within MR1 molecules produced by tumor cells and their abundance and antigenicity were enhanced by drugs that induce carbonyl accumulation. Our data reveal carbonyl nucleobase adducts as MR1T cell antigens. Recognizing cells under carbonyl stress allows MR1T cells to monitor cellular metabolic changes with physiological and therapeutic implications.

2024-05-11 | GSE160366 | GEO

ILC2s directly activate anti-tumor cytotoxic CD8+ T lymphocytes by internalizing, processing, and presenting exogenous antigens

Project description:ILC2s directly activate anti-tumor cytotoxic CD8+ T lymphocytes by internalizing, processing, and presenting exogenous antigens

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Immunoglobulin expression in the endoplasmic reticulum shapes the metabolic fitness of B lymphocytes

Project description:The major function of B lymphocytes is to sense antigens and to produce protective antibodies after activation. This function requires the expression of a B-cell antigen receptor (BCR), and evolutionary conserved mechanisms seem to exist that ensure that B cells without a BCR do not develop nor survive in the periphery. Here, we show that the loss of BCR expression on Burkitt lymphoma cells leads to decreased mitochondrial function and impaired metabolic flexibility. Strikingly, this phenotype does not result from the absence of a classical Syk-dependent BCR signal but rather from compromised ER expansion. We show that the reexpression of immunoglobulins (Ig) in the absence of the BCR signaling subunits Igα and Igβ rescues the observed metabolic defects. We demonstrate that immunoglobulin expression is needed to maintain ER homeostasis not only in lymphoma cells but also in resting B cells. Our study provides evidence that the expression of BCR components, which is sensed in the ER and shapes mitochondrial function, represents a novel mechanism of metabolic control in B cells.

2020-04-21 | MTBLS186 | MetaboLights

Microbial Antigens Stimulate Metalloprotease-7 Secretion in Human B-Lymphocytes Using mTOR-Dependent and Independent Pathways.

Project description:Metalloproteinases (MMPs) contribute to tissue remodeling and acute inflammation not only by degrading extracellular matrix proteins but also by controlling the influx of chemokines through the regulation and shedding of syndecans. B-lymphocytes, in addition to their well-known function as antibody producing cells, participate in the innate immune response by secreting inflammatory cytokines and chemokines. However, there is little information about the role of B-lymphocytes in the regulation of MMPs; consequently, herein we investigated whether activated human circulating B-lymphocytes contributed to the secretion of MMPs. We demonstrate that B-lymphocytes activated by un-methylated CpG motifs, found in bacterial DNA, and β-glucans, found in the cell wall of fungi, both induced MMP-7. Interestingly, while CpG-stimulated cells activated the mTOR pathway via TLR9 receptor to induced MMP-7, β-glucan-stimulated cells were mTOR-independent and used Dectin-1 receptor. B-lymphocytes did not seem to have a major role in the secretion of tissue inhibitors of metalloproteinases (TIMPs). However, secreted MMP-7 participated in the shedding of Syndecan-4 from the surface of B-lymphocytes. In conclusion, circulating human B-lymphocytes contribute to the regulation of the innate immune system by participating in the secretion of MMP-7 which in turn is important for the shedding of Syndecan-4 in response to infectious stimuli.

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