scholarly journals Depletion of Collagen IX Alpha1 Impairs Myeloid Cell Function

Stem Cells ◽  
2018 ◽  
Vol 36 (11) ◽  
pp. 1752-1763 ◽  
Author(s):  
Kristina Probst ◽  
Jacek Stermann ◽  
Inga von Bomhard ◽  
Julia Etich ◽  
Lena Pitzler ◽  
...  
Keyword(s):  
Cell Function ◽  
Myeloid Cell ◽  
Collagen Ix

scholarly journals Regulation of Myeloid Cell Function through the CD200 Receptor

2005 ◽  
Vol 176 (1) ◽  
pp. 191-199 ◽  
Author(s):  
Maria C. Jenmalm ◽  
Holly Cherwinski ◽  
Edward P. Bowman ◽  
Joseph H. Phillips ◽  
Jonathon D. Sedgwick
Keyword(s):  
Cell Function ◽  
Myeloid Cell ◽  
Cd200 Receptor

scholarly journals Transcription factor Gfi-1 induced by G-CSF is a negative regulator of CXCR4 in myeloid cells

Blood ◽  
2007 ◽  
Vol 110 (7) ◽  
pp. 2276-2285 ◽  
Author(s):  
Maria De La Luz Sierra ◽  
Paola Gasperini ◽  
Peter J. McCormick ◽  
Jinfang Zhu ◽  
Giovanna Tosato
Keyword(s):  
Bone Marrow ◽  
Dna Sequences ◽  
Peripheral Blood ◽  
Cell Function ◽  
Myeloid Cell ◽  
Cxcr4 Expression ◽  
Negative Regulator ◽  
Hematopoietic Stem

The mechanisms underlying granulocyte-colony stimulating factor (G-CSF)–induced mobilization of granulocytic lineage cells from the bone marrow to the peripheral blood remain elusive. We provide evidence that the transcriptional repressor growth factor independence-1 (Gfi-1) is involved in G-CSF–induced mobilization of granulocytic lineage cells from the bone marrow to the peripheral blood. We show that in vitro and in vivo G-CSF promotes expression of Gfi-1 and down-regulates expression of CXCR4, a chemokine receptor essential for the retention of hematopoietic stem cells and granulocytic cells in the bone marrow. Gfi-1 binds to DNA sequences upstream of the CXCR4 gene and represses CXCR4 expression in myeloid lineage cells. As a consequence, myeloid cell responses to the CXCR4 unique ligand SDF-1 are reduced. Thus, Gfi-1 not only regulates hematopoietic stem cell function and myeloid cell development but also probably promotes the release of granulocytic lineage cells from the bone marrow to the peripheral blood by reducing CXCR4 expression and function.

scholarly journals Myeloid-derived suppressor cell function and epigenetic expression evolves over time after surgical sepsis

Critical Care ◽  
2019 ◽  
Vol 23 (1) ◽  
Author(s):  
McKenzie K. Hollen ◽  
Julie A. Stortz ◽  
Dijoia Darden ◽  
Marvin L. Dirain ◽  
Dina C. Nacionales ◽  
...  
Keyword(s):  
Cell Function ◽  
Expression Patterns ◽  
Suppressor Cells ◽  
Myeloid Cell ◽  
Suppressor Cell ◽  
Myeloid Derived Suppressor Cell ◽  
T Lymphocyte Proliferation ◽  
Suppressive Phenotype ◽  
Sepsis Survivors ◽  
Over Time

Abstract Background Sepsis is an increasingly significant challenge throughout the world as one of the major causes of patient morbidity and mortality. Central to the host immunologic response to sepsis is the increase in circulating myeloid-derived suppressor cells (MDSCs), which have been demonstrated to be present and independently associated with poor long-term clinical outcomes. MDSCs are plastic cells and potentially modifiable, particularly through epigenetic interventions. The objective of this study was to determine how the suppressive phenotype of MDSCs evolves after sepsis in surgical ICU patients, as well as to identify epigenetic differences in MDSCs that may explain these changes. Methods Circulating MDSCs from 267 survivors of surgical sepsis were phenotyped at various intervals over 6 weeks, and highly enriched MDSCs from 23 of these samples were co-cultured with CD3/CD28-stimulated autologous T cells. microRNA expression from enriched MDSCs was also identified. Results We observed that MDSC numbers remain significantly elevated in hospitalized sepsis survivors for at least 6 weeks after their infection. However, only MDSCs obtained at and beyond 14 days post-sepsis significantly suppressed T lymphocyte proliferation and IL-2 production. These same MDSCs displayed unique epigenetic (miRNA) expression patterns compared to earlier time points. Conclusions We conclude that in sepsis survivors, immature myeloid cell numbers are increased but the immune suppressive function specific to MDSCs develops over time, and this is associated with a specific epigenome. These findings may explain the chronic and persistent immune suppression seen in these subjects.

scholarly journals Granulocytic Myeloid-Derived Suppressor Cells Aggravate Tuberculosis Caused by Hypervirulent Mycobacteria

2020 ◽  
Author(s):  
Caio César Barbosa Bomfim ◽  
Eduardo Pinheiro Amaral ◽  
Igor Santiago-Carvalho ◽  
Gislane Almeida Santos ◽  
Érika Machado Salles ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
Cell Function ◽  
Pulmonary Inflammation ◽  
Bacterial Load ◽  
Suppressor Cells ◽  
Myeloid Cell ◽  
Partial Recovery ◽  
Myeloid Derived Suppressor Cells

Abstract Background The role of myeloid-derived suppressor cells (MDSCs) in severe tuberculosis patients who suffer from uncontrolled pulmonary inflammation caused by hypervirulent mycobacterial infection remains unclear. Methods This issue was addressed using C57BL/6 mice infected with highly virulent Mycobacterium bovis strain MP287/03. Results CD11b +GR1 int population increased in the bone marrow, blood and lungs during advanced disease. Pulmonary CD11b +GR1 int (Ly6G intLy6C int) cells showed granularity similar to neutrophils and expressed immature myeloid cell markers. These immature neutrophils harbored intracellular bacilli and were preferentially located in the alveoli. T cell suppression occurred concomitantly with CD11b +GR1 int cell accumulation in the lungs. Furthermore, lung and bone-marrow GR1 + cells suppressed both T cell proliferation and IFN-γ production in vitro. Anti-GR1 therapy given when MDSCs infiltrated the lungs prevented expansion and fusion of primary pulmonary lesions and the development of intragranulomatous caseous necrosis, along with increased mouse survival and partial recovery of T cell function. Lung bacterial load was reduced by anti-GR1 treatment, but mycobacteria released from the depleted cells proliferated extracellularly in the alveoli, forming cords and clumps. Conclusions Granulocytic MDSCs massively infiltrate the lungs during infection with hypervirulent mycobacteria, promoting bacterial growth and the development of inflammatory and necrotic lesions, and are promising targets for host-directed therapies.

scholarly journals Interleukin‐6‐mediated resistance to immunotherapy is linked to impaired myeloid cell function

2020 ◽  
Vol 148 (1) ◽  
pp. 211-225 ◽  
Author(s):  
Elham Beyranvand Nejad ◽  
Camilla Labrie ◽  
Tetje C. Sluis ◽  
Suzanne Duikeren ◽  
Kees L. M. C. Franken ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Cell Function ◽  
Myeloid Cell

scholarly journals Influenza Vaccination Primes Human Myeloid Cell Cytokine Secretion and NK Cell Function

2019 ◽  
Vol 203 (6) ◽  
pp. 1609-1618 ◽  
Author(s):  
Helen R. Wagstaffe ◽  
Harry Pickering ◽  
Joanna Houghton ◽  
Jason P. Mooney ◽  
Asia-Sophia Wolf ◽  
...  
Keyword(s):  
Influenza Vaccination ◽  
Cell Function ◽  
Nk Cell ◽  
Myeloid Cell ◽  
Cytokine Secretion

scholarly journals Inhibition of Caveolin-1 Restores Myeloid Cell Function in Human Glioblastoma

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e77397 ◽  
Author(s):  
Shinji Shimato ◽  
Lisa M. Anderson ◽  
Martin Asslaber ◽  
Jeffrey N. Bruce ◽  
Peter Canoll ◽  
...  
Keyword(s):  
Cell Function ◽  
Myeloid Cell ◽  
Human Glioblastoma ◽  
Caveolin 1

scholarly journals Malaria Parasite Infection Compromises Control of Concurrent Systemic Non-typhoidal Salmonella Infection via IL-10-Mediated Alteration of Myeloid Cell Function

2014 ◽  
Vol 10 (5) ◽  
pp. e1004049 ◽  
Author(s):  
Kristen L. Lokken ◽  
Jason P. Mooney ◽  
Brian P. Butler ◽  
Mariana N. Xavier ◽  
Jennifer Y. Chau ◽  
...  
Keyword(s):  
Malaria Parasite ◽  
Cell Function ◽  
Myeloid Cell ◽  
Parasite Infection ◽  
Salmonella Infection ◽  
Malaria Parasite Infection
Sign in / Sign up

Export Citation Format

Share Document