Sentences with phrase «with lymphoid cells»

Thus, blood cells can become sensitive to this death pathway if they come into contact with lymphoid cells, as would occur when blood CD4 T cells traffic into lymphoid tissues.

Purpose of Study: Recent studies in dogs with lymphoid cell neoplasia have demonstrated the safety and efficacy of Tanovea - CA1 ™ and have led to its conditional FDA approval.

Not exact matches

Consistent with this idea, microscopic examination of fetal small intestine before birth reveals immature epithelium and sparse lymphoid cells.

Using lymphoid tissue infected with HIV, the scientists compared cell death rates between cell - to - cell and cell - free virus transfer.

When injected together with factor VIII into mouse models of haemophilia A, the nanoparticles deliver their payload to cells in the lymphoid tissue that are responsible for initiating immune responses.

The researchers deleted the HIC1 gene in certain innate lymphoid cells in the mouse intestine and found that this increased the susceptibility of the mice to infection with the bacterium Citrobacter rodentium.

Gregory F. Sonnenberg, PhD, research associate in the Department of Medicine, Gastroenterology Division, and the Institute for Immunology at the Perelman School of Medicine, University of Pennsylvania, with postdoctoral researcher Matthew Hepworth, PhD, report in Nature that innate lymphoid cells (ILCs) directly limit the response by inflammatory T cells to commensal bacteria in the gut of mice.

«These findings will make it possible to significantly improve the quality of treatment of rheumatoid arthritis in future with the help of innate lymphoid cells,» says Dr Ramming.

The research team, a collaborative partnership between the groups of Professor Gabrielle Belz of Melbourne's Walter and Eliza Hall Institute, and Professor Eric Vivier at the Centre d'Immunologie de Marseille - Luminy, France, found that innate lymphoid cells (ILCs) are crucial for protecting against bacterial infection in people with compromised immune systems.

In humans, Newcomb and her colleagues measured the number of group 2 innate lymphoid cells circulating in the blood of adults with moderate to severe asthma.

Adult male mice also started off with fewer of the lymphoid cells in the lungs than adult females, the researchers found: Female mice had about 1 1/2 times as many of these immune cells as males.

The frequency of CD39highCD8 + T cells increased with tumor growth but was absent in lymphoid organs.

Diagnosis of BPDCN was confirmed by the positivity of the cells for CD4 and CD56, along with other markers that are more restricted to plasmacytoid dendritic cells (such as CD123), and the negativity of the cells for lymphoid, NK and myeloid lineage - associated antigens.

In pathological conditions, MSCs migrate preferentially into lymphoid organs, allografts, injured and / or inflammatory tissue sites after systemic transfusion, where they interact with the activated immune cells and modulate their function 51, 52.

In a curious twist resembling cellular alchemy, when blood T cells are cultured with lymphoid tissue from the tonsils or spleen, the blood T cells begin acting like lymphoid tissue T cells, becoming more activated and more susceptible to abortive infection and death by pyroptosis.

The group of promoters, whose H3K4me3 levels were affected by combined chidamide and decitabine treatment, but not by either chidamide or decitabine treatment alone, was enriched with binding site motifs for PU.1, a transcription factor that activates gene expression during myeloid and B - cell lymphoid cell development15, 16 (Figure 5C).

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.

FITC + LC / DC sorted from the LNs of lymphoid deficient or control mice stimulated naive T cells with similar efficiency.

This hematoxylin and eosin stained slide of a surgically removed (resected) primary pancreatic tumor shows a cluster of immune cells (lymphoid aggregate) observed next to a pancreatic tumor lesion in a patient treated with a GM - CSF vaccine 2 weeks before surgical removal of the primary tumor.

Susan Amara, USA - «Regulation of transporter function and trafficking by amphetamines, Structure - function relationships in excitatory amino acid transporters (EAATs), Modulation of dopamine transporters (DAT) by GPCRs, Genetics and functional analyses of human trace amine receptors» Tom I. Bonner, USA (Past Core Member)- Genomics, G protein coupled receptors Michel Bouvier, Canada - Molecular Pharmacology of G protein - Coupled Receptors; Molecular mechanisms controlling the selectivity and efficacy of GPCR signalling Thomas Burris, USA - Nuclear Receptor Pharmacology and Drug Discovery William A. Catterall, USA (Past Core Member)- The Molecular Basis of Electrical Excitability Steven Charlton, UK - Molecular Pharmacology and Drug Discovery Moses Chao, USA - Mechanisms of Neurotophin Receptor Signaling Mark Coles, UK - Cellular differentiation, human embryonic stem cells, stromal cells, haematopoietic stem cells, organogenesis, lymphoid microenvironments, develomental immunology Steven L. Colletti, USA Graham L Collingridge, UK Philippe Delerive, France - Metabolic Research (diabetes, obesity, non-alcoholic fatty liver, cardio - vascular diseases, nuclear hormone receptor, GPCRs, kinases) Sir Colin T. Dollery, UK (Founder and Past Core Member) Richard M. Eglen, UK Stephen M. Foord, UK David Gloriam, Denmark - GPCRs, databases, computational drug design, orphan recetpors Gillian Gray, UK Debbie Hay, New Zealand - G protein - coupled receptors, peptide receptors, CGRP, Amylin, Adrenomedullin, Migraine, Diabetes / obesity Allyn C. Howlett, USA Franz Hofmann, Germany - Voltage dependent calcium channels and the positive inotropic effect of beta adrenergic stimulation; cardiovascular function of cGMP protein kinase Yu Huang, Hong Kong - Endothelial and Metabolic Dysfunction, and Novel Biomarkers in Diabetes, Hypertension, Dyslipidemia and Estrogen Deficiency, Endothelium - derived Contracting Factors in the Regulation of Vascular Tone, Adipose Tissue Regulation of Vascular Function in Obesity, Diabetes and Hypertension, Pharmacological Characterization of New Anti-diabetic and Anti-hypertensive Drugs, Hypotensive and antioxidant Actions of Biologically Active Components of Traditional Chinese Herbs and Natural Plants including Polypehnols and Ginsenosides Adriaan P. IJzerman, The Netherlands - G protein - coupled receptors; allosteric modulation; binding kinetics Michael F Jarvis, USA - Purines and Purinergic Receptors and Voltage-gated ion channel (sodium and calcium) pharmacology Pain mechanisms Research Reproducibility Bong - Kiun Kaang, Korea - G protein - coupled receptors; Glutamate receptors; Neuropsychiatric disorders Eamonn Kelly, Prof, UK - Molecular Pharmacology of G protein - coupled receptors, in particular opioid receptors, regulation of GPCRs by kinasis and arrestins Terry Kenakin, USA - Drug receptor pharmacodynamics, receptor theory Janos Kiss, Hungary - Neurodegenerative disorders, Alzheimer's disease Stefan Knapp, Germany - Rational design of highly selective inhibitors (so call chemical probes) targeting protein kinases as well as protein interaction inhibitors of the bromodomain family Andrew Knight, UK Chris Langmead, Australia - Drug discovery, GPCRs, neuroscience and analytical pharmacology Vincent Laudet, France (Past Core Member)- Evolution of the Nuclear Receptor / Ligand couple Margaret R. MacLean, UK - Serotonin, endothelin, estrogen, microRNAs and pulmonary hyperten Neil Marrion, UK - Calcium - activated potassium channels, neuronal excitability Fiona Marshall, UK - GPCR molecular pharmacology, structure and drug discovery Alistair Mathie, UK - Ion channel structure, function and regulation, pain and the nervous system Ian McGrath, UK - Adrenoceptors; autonomic transmission; vascular pharmacology Graeme Milligan, UK - Structure, function and regulation of G protein - coupled receptors Richard Neubig, USA (Past Core Member)- G protein signaling; academic drug discovery Stefan Offermanns, Germany - G protein - coupled receptors, vascular / metabolic signaling Richard Olsen, USA - Structure and function of GABA - A receptors; mode of action of GABAergic drugs including general anesthetics and ethanol Jean - Philippe Pin, France (Past Core Member)- GPCR - mGLuR - GABAB - structure function relationship - pharmacology - biophysics Helgi Schiöth, Sweden David Searls, USA - Bioinformatics Graeme Semple, USA - GPCR Medicinal Chemistry Patrick M. Sexton, Australia - G protein - coupled receptors Roland Staal, USA - Microglia and neuroinflammation in neuropathic pain and neurological disorders Bart Staels, France - Nuclear receptor signaling in metabolic and cardiovascular diseases Katerina Tiligada, Greece - Immunopharmacology, histamine, histamine receptors, hypersensitivity, drug allergy, inflammation Georg Terstappen, Germany - Drug discovery for neurodegenerative diseases with a focus on AD Mary Vore, USA - Activity and regulation of expression and function of the ATP - binding cassette (ABC) transporters

Venous blood was drawn at these time points and the cells stained with PE - conjugated antibodies against MHC class I, class II, CD45, CD3, B220 or Gr - 1, which represent antibodies against myeloid and lymphoid markers.

Perhaps the greatest attraction and chief benefit of intratumoral therapies is their ability to synergize with systemic checkpoint therapies and accelerate the development of a lymphoid infiltrate and perhaps secondary lymphoid structures in vivo, which in turn can result in systemic mobilization of a T - cell response: the local injection — global effect model.

With 70 % of it housed in the Gut Associated Lymphoid Tissue (GALT) in the intestinal wall, the ecosystem of microbial residents are responsible for influencing the immune gatekeepers such as dendritic cells.

Tissue overgrowth (hyperplasia), either of lymphoid cells or macrophages with fibrous tissue (fibrohistiocytic nodules) is also common.