Sentences with phrase «myeloid cell development»

Areas of particular interest are host - pathogen interactions, pattern recognition receptors, cellular signaling and immunometabolism, and myeloid cell development.

Not exact matches

In this study, published in the journal Cell Reports, and led by Dr. Esteban Ballestar (IDIBELL), the comparison of the epigenetic profiles between dendritic cells and myeloid - derived suppressor cells has allowed them to identify the existence of specific epigenetic alterations that associated with the development of myeloid - derived suppressor cells as a result of exposure to prostaglandin E2.

A few years ago, Singh and colleagues identified a transcription factor called PU.1 that acts as the primary signal, a central genetic switch to initiate development of myeloid progenitor cells.

Anna Huttenlocher, University of Wisconsin, USA Neutrophils in the Tumor Microenvironment Neutrophils, Wounds, and Cancer Progression Stefan Kaufmann, Max Planck Institute, Germany Pathology and immune reactivity: understanding multidimensionality in pulmonary tuberculosis Constitutive BAK activation as a determinant of drug sensitivity in malignant lymphohematopoietic cells Kathryn Moore, New York University, USA MicroRNA -33-dependent regulation of macrophage metabolism directs immune cell polarization in atherosclerosis Lalita Ramakrishnan, University of Cambridge, UK Myeloid Growth Factors Promote Resistance to Mycobacterial Infection by Curtailing Granuloma Necrosis through Macrophage Replenishment Beth Stevens, Harvard University, USA Microglia: Dynamic Mediators of Synapse Development and Plasticity Do glia drive synaptic and cognitive impairment in disease?

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.

Hypoxia Inducible Factor - 1α in Astrocytes and / or Myeloid Cells Is Not Required for the Development of Autoimmune Demyelinating Disease

Myeloid cells are cells that would have become other blood cells (white blood cells other than lymphocytes, red blood cells or platelets) under normal development.

Their system was based on earlier studies in which Singh and his colleagues identified a transcription factor called PU.1 as a central genetic switch that triggers development of myeloid progenitor cells.

His lab has made contributions in the area of tumor induced immunosuppression of dendritic cells, characterization of human myeloid derived suppressor cells, and the development of novel adjuvants for cancer vaccines.

Loss of prolyl hydroxylase - 2 in myeloid cells and T - lymphocytes impairs tumor development.

The project «Preprogrammed versus stochastic clonal evolution of relapsing Acute Myeloid Leukaemia: Impact on disease development and therapeutic responses» will dissect why the subpopulations of primary human blood cancer cells that drive leukaemic relapse resist relevant clinical treatments in vivo.