Sentences with phrase «t cells involved»

Our findings show that two fragments of alpha - synuclein, a protein that accumulates in the brain cells of people with Parkinson's, can activate the T cells involved in autoimmune attacks.

Not exact matches

The trial involved an experimental checkpoint inhibitor from Bristol - Myers Squibb called ipilimumab (now marketed as Yervoy)-- whose aim was to release the molecular brakes on her own army of T cells.

Basically, CAR - T therapy involves taking a patient's own immune «killer» T - cells, inserting new genetic code into those cells which turn them into cancer - hunters that can home in on malignant B - cells (another kind of immune cell), and then pumping these specialized leukemia - busting cells back into the patient.

In clinical trials the treatment — which involves extracting individual patients» immune T - cells, modifying them to seek out tell - tale biological markers associated with blood cancers like aggressive lymphoma, and then pumping those modified killer cells back into the body — has shown major promise, in some cases eliminating all signs of the cancer in patients six months after treatment.

Those two companies, along with their larger competitor Novartis (nvs), are developing experimental chimeric antigen receptor T - cell (CAR - T) technology platforms, which are highly personalized treatments that involve extracting patients» immune cells, re-engineering them to target their specific cancers, and then pumping these sniper - cells back into the body.

The novel treatment space involves transforming a patient's own immune T - cells into cancer - busting weapons.

Bellicum is among the flurry of biotechs investing heavily into cell therapies such as experimental chimeric antigen receptor T - cell (CAR - T) treatments for cancer (this is the next - gen treatment that involves reprogramming immune cells to become cancer killers and has shown promise in blood cancers, which Bellicum specializes in).

Regulators noted that they will require special training for anyone involved in delivering this therapy, while expanding the approval of Actemra (tocilizumab) to treat CAR T - cell - induced severe or life - threatening CRS in patients 2 years of age or older.

CAR - T approaches involve reengineering T - cells to find and destroy cancer cells, but that process can cause cytokine release syndrome (CRS), a life - threatening immune response NantKwest hopes to sidestep.

The research involved using novel technologies to examine the T cells in human tissues.

Although the researchers emphasized that laboratory results involving cell lines and mice do not necessarily translate to human treatment, they say their findings show that new mTOR inhibitors combined with chemotherapy could become a new treatment strategy for T - ALL.

In the meantime, the MUSC team, led by Yu, will continue their work and try to extend the current findings by investigating how other miRs may be involved in regulating T - and B - cell function during allogeneic BMT.

Oral immunotherapy for peanut allergy induces early, distinct changes in immune T - cell populations that potentially may help researchers determine which people will respond well to the therapy and which immune mechanisms are involved in the response, a new study suggests.

«So, we not only found a new mechanism for cGVHD development by demonstrating that this miR -17-92 is heavily involved in the T - and B - cell responses that lead to cGVHD, but we also found that blocking miR - 17 substantially reduced cGVHD symptoms in mice.

The work «implicates this regulatory T cell as being involved in atherosclerosis,» says Alan Daugherty, head of the cardiovascular research center at the University of Kentucky in Lexington.

The first key experiment involved removing a specific subset of activated T - cells from mouse models.

With chronically infected mice as their model, the researchers used a new technology called ATAC - seq to map the regulatory regions of the genome — the sections of DNA involved in switching genes on and off — in the animals» exhausted and functional CD8 + T cells.

'' (T) he immune response involves reprogramming the entire cell and also often the entire plant,» Cann said.»

To address such obstacles, Roybal, now an assistant professor at the University of California, San Francisco and his colleague Leonardo Morsut turned to a signaling molecule on T cells called the Notch receptor, known to be involved in several developmental and biological processes.

TB is known for trying to block activation of T cells by infected dendritic cells, two kinds of which are primarily involved in fighting infection: dendritic cells that migrate from the lungs to the lymph nodes, and those that already reside in the lymph nodes.

The researchers are now looking at how ICOS signals can be altered to diminish autoimmune disorders and augmented for more effective vaccine development, and are beginning research on how ICOS signaling may benefit Chimeric Antigen Receptor - T cell (CAR - T) therapies, which involves engineering of patient's own immune cells to recognize and attack their cancers.

Indeed, when mice lacking the gene for making IL - 4 take the water maze test, they do badly, perhaps because their T cells lack a critical signal involved in fast learning.

Many different cells are involved in the complex processes: skin cells (keratinocytes) and cells of the immune system, among others T lymphocytes, macrophages, mast cells and others.

On top of the T cell abnormalities, chronic GVHD involves antibody - producing B cells and scavenger cells called macrophages.

John Rossi, a molecular biologist at the Beckman Research Institute in Duarte, Calif., who was not involved in the research, noted that from his own work, using RNAi to treat T cells may allow patients to significantly reduce the dosage of the anti-HIV drugs — up to 100-fold.

Severe disease is thought to result from immunopathogenic processes involving serotype cross-reactive antibodies and T cells that together induce vasoactive cytokines, causing vascular leakage that leads to shock.

A unique approach to targeting the abnormal T - cells that cause T - cell lymphomas could offer hope to patients with the aggressive and difficult - to - treat family of cancers, finds a study involving researchers from Cardiff University.

Rejection by CD8 + T cells does not appear to involve either allospecific CTL or DTH effector mechanisms; however, CD8 + T cells are able to induce significant apoptosis of allogeneic corneal endothelial cells.

New blood cancer breakthroughs — including several involving CAR T cell therapy — were announced by City of Hope physicians at the American Society of Hematology (ASH) annual meeting in Atlanta.

The present findings are derived from studies using CD4KO mice and thus, raise the question as to whether the CD4 + T cell - independent immune mechanisms in CD4 KO mice differ from those involved in corneal allograft rejection in wild - type mice whose CD4 + T cells population have been depleted with monoclonal antibodies.

In CD4 KO mice, T cell - independent rejection can involve either CD8 + or CD8 − T cells.

T - cell therapy involves genetically re-engineering a type of the patient's own disease - fighting white blood cells, called T - cells, to fight cancer.

«This immunosuppressive tumor microenvironment involves CD4 + and FoxP3 + cells that represent a regulatory T - cell population.

A Marked Reduction in Priming of Cytotoxic CD8 + T Cells Mediated by Stress - Induced Glucocorticoids Involves Multiple Deficiencies in Cross-Presentation by Dendritic Cells.

That approach targets the PD - 1 protein, which is involved in a complex process that prevents the immune system's T - cells from attacking cancer.

Identification of human T cell leukemia virus type 1 tax amino acid signals and cellular factors involved in secretion of the viral oncoprotein.

Interaction of human mesenchymal stem cells with cells involved in alloantigen - specific immune response favors the differentiation of CD4 + T - cell subsets expressing a regulatory / suppressive phenotype.

In one study involving nineteen patients, Coukos found that one - third had T cells in their blood that recognized their tumors.

The approach is very unique and involves targeting the chemokine molecule CCR5 in patient's T - cells by ZNFs.

CAR - T immunotherapy involves genetically outfitting a patient's immune cells with a new artificial gene, a chimeric antigen receptor (CAR), which allows the cells to recognize and attack specific cancer cells.

His plans for research in his own lab involve «continuing to look at the mechanisms of T cell dysfunction in human and mice.

«We knew that TET proteins were involved in human cancer but we didn't know how they regulated T cell development,» says Angeliki Tsagaratou, Ph.D., an instructor in the Rao lab and the study's first author.

Clinical trials involving CAR - T cells have offered cancer patients who have exhausted traditional chemotherapy treatment options a new lease on life.

T cells exert their actions in two ways, either through direct cell - cell contact which involves transmembrane proteins present on both the T cell and interacting cell, or by the secretion of soluble proteins termed cytokines which have receptors on many lymphoid and some non-lymphoid cell types.

This finding recapitulated the features of many human blood cancers, including those involving T cells, in which TET2 is often mutated or lost.

Allogeneic cell therapies involving primary cell types such as bone marrow mesenchymal stromal / stem cells (BM - MSCs), hematopoietic stem and progenitor cells (HSPCs), and T and natural killer (NK) cells for immunotherapy applications are especially challenging because of the vigorous process of screening...

GVHD is an immune - mediated disease in which donor T cells recognize and attack the histocompatibility - disparate recipient; it involves multiple organs, such as the lung, liver, intestinal tract, and skin (2 — 4).

This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.

One of these modifications, O - GlcNAc, is known to be involved in the activation of T cells; however, its function on most glycoproteins remains unknown due to difficulty in characterizing and mapping O - GlcNAc sites.

Nodal Involvement By Marginal Zone B - Cell Lymphoma Harboring t (14; 22)(q32; q11) Involving Immunoglobulin Heavy Chain and Light Chain Lambda as the Sole Karyotypically Recognizable Abnormality in a...