scholarly journals A2B adenosine receptor activation switches differentiation of bone marrow cells to a CD11c + Gr‐1 + dendritic cell subset that promotes the Th17 response

2015 ◽  
Vol 3 (4) ◽  
pp. 360-373 ◽  
Author(s):  
Dongchun Liang ◽  
Aijun Zuo ◽  
Hui Shao ◽  
Mingjiazi Chen ◽  
Henry J. Kaplan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cell ◽  
Adenosine Receptor ◽  
Bone Marrow Cells ◽  
Cell Subset ◽  
Receptor Activation ◽  
Dendritic Cell Subset ◽  
Th17 Response ◽  
A2b Adenosine Receptor ◽  
Adenosine Receptor Activation

scholarly journals IL-4 supports the generation of a dendritic cell subset from murine bone marrow with altered endocytosis capacity

2004 ◽  
Vol 77 (4) ◽  
pp. 535-543 ◽  
Author(s):  
Mauritius Menges ◽  
Thomas Baumeister ◽  
Susanne Rössner ◽  
Patrizia Stoitzner ◽  
Nikolaus Romani ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cell ◽  
Cell Subset ◽  
Dendritic Cell Subset ◽  
Murine Bone Marrow

scholarly journals Early adenosine receptor activation ameliorates spinal cord reperfusion injury

2008 ◽  
Vol 9 (4) ◽  
pp. 363-367 ◽  
Author(s):  
T Brett Reece ◽  
Curtis G Tribble ◽  
David O Okonkwo ◽  
Jonathon D Davis ◽  
Thomas S Maxey ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Reperfusion Injury ◽  
Adenosine Receptor ◽  
Receptor Activation ◽  
Adenosine Receptor Activation

scholarly journals Heme-stress activated NRF2 skews fate trajectories of bone marrow cells from dendritic cells towards red pulp-like macrophages in hemolytic anemia

2022 ◽  
Author(s):  
Florence Vallelian ◽  
Raphael M. Buzzi ◽  
Marc Pfefferlé ◽  
Ayla Yalamanoglu ◽  
Irina L. Dubach ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
Dendritic Cell ◽  
Sickle Cell Disease ◽  
Bone Marrow Cells ◽  
Cell Disease ◽  
Secondary Immunodeficiency ◽  
Gm Csf ◽  
Bone Marrow Cultures ◽  
Marrow Cultures

AbstractHeme is an erythrocyte-derived toxin that drives disease progression in hemolytic anemias, such as sickle cell disease. During hemolysis, specialized bone marrow-derived macrophages with a high heme-metabolism capacity orchestrate disease adaptation by removing damaged erythrocytes and heme-protein complexes from the blood and supporting iron recycling for erythropoiesis. Since chronic heme-stress is noxious for macrophages, erythrophagocytes in the spleen are continuously replenished from bone marrow-derived progenitors. Here, we hypothesized that adaptation to heme stress progressively shifts differentiation trajectories of bone marrow progenitors to expand the capacity of heme-handling monocyte-derived macrophages at the expense of the homeostatic generation of dendritic cells, which emerge from shared myeloid precursors. This heme-induced redirection of differentiation trajectories may contribute to hemolysis-induced secondary immunodeficiency. We performed single-cell RNA-sequencing with directional RNA velocity analysis of GM-CSF-supplemented mouse bone marrow cultures to assess myeloid differentiation under heme stress. We found that heme-activated NRF2 signaling shifted the differentiation of bone marrow cells towards antioxidant, iron-recycling macrophages, suppressing the generation of dendritic cells in heme-exposed bone marrow cultures. Heme eliminated the capacity of GM-CSF-supplemented bone marrow cultures to activate antigen-specific CD4 T cells. The generation of functionally competent dendritic cells was restored by NRF2 loss. The heme-induced phenotype of macrophage expansion with concurrent dendritic cell depletion was reproduced in hemolytic mice with sickle cell disease and spherocytosis and associated with reduced dendritic cell functions in the spleen. Our data provide a novel mechanistic underpinning of hemolytic stress as a driver of hyposplenism-related secondary immunodeficiency.

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