scholarly journals Generation or large numbers of immature and mature dendritic cells from rat bone marrow cultures

1998 ◽  
Vol 28 (3) ◽  
pp. 811-817 ◽  
Author(s):  
Mia Talmor ◽  
Asra Mirza ◽  
Shannon Turley ◽  
Ira Mellman ◽  
Lloyd A. Hoffman ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
Large Numbers ◽  
Bone Marrow Cultures ◽  
Marrow Cultures ◽  
Rat Bone

scholarly journals Differentiation of dendritic cells in cultures of rat bone marrow cells.

1986 ◽  
Vol 163 (4) ◽  
pp. 872-883 ◽  
Author(s):  
W E Bowers ◽  
M R Berkowitz
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
Bone Marrow Cells ◽  
Sensitive Assay ◽  
Ia Antigens ◽  
Bone Marrow Cultures ◽  
Nonadherent Cells ◽  
Marrow Cultures ◽  
Rat Bone ◽  
Marrow Cells

Although dendritic cells (DC) originate from bone marrow, they were not observed in fresh preparations of bone marrow cells (BMC). Likewise, accessory activity was barely measurable in a sensitive assay for this potent function of DC. However, both DC and accessory activity developed when BMC were cultured for 5 d. Based on fractionation before culture, nearly all of the accessory activity could be attributed to only 5% of the total BMC recovered in a low-density (LD) fraction. The LD-DC precursors differed from mature DC in a number of important respects. Removal of Ia+ cells from the LD fraction by panning did not decrease the production of DC when the nonadherent cells were cultured. Thus, the cell from which the DC is derived does not express or minimally expresses Ia antigens, in contrast to the strongly Ia+ DC that is produced in bone marrow cultures. Irradiation of LD cells before culture prevented the development of DC. When irradiation was delayed by daily intervals, progressive increases in the number of DC resulted, up to the fifth day. These findings, together with preliminary autoradiographic data, indicate that cell division has occurred, in contrast to the DC, which does not divide. We conclude that bone marrow-derived DC arise in culture from the division of LD, Ia- precursors.

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.

scholarly journals Murine Plasmacytoid Pre-Dendritic Cells Generated from Flt3 Ligand-Supplemented Bone Marrow Cultures Are Immature APCs

2002 ◽  
Vol 169 (12) ◽  
pp. 6711-6719 ◽  
Author(s):  
Pierre Brawand ◽  
David R. Fitzpatrick ◽  
Brad W. Greenfield ◽  
Kenneth Brasel ◽  
Charles R. Maliszewski ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
Flt3 Ligand ◽  
Bone Marrow Cultures ◽  
Marrow Cultures

Stromal components in rat bone marrow frozen sections compared to long-term rat bone marrow cultures

1995 ◽  
Vol 5 (2) ◽  
pp. 69-78
Author(s):  
E. Barb� ◽  
J. G. M. C. Damoiseaux ◽  
E. A. D�pp ◽  
C. D. Dijkstra
Keyword(s):  
Bone Marrow ◽  
Frozen Sections ◽  
Bone Marrow Cultures ◽  
Marrow Cultures ◽  
Rat Bone

scholarly journals Role of colony-stimulating activity in murine long-term bone marrow cultures: evidence for its production and consumption by the adherent cells

Blood ◽  
1982 ◽  
Vol 59 (4) ◽  
pp. 761-767 ◽  
Author(s):  
JM Heard ◽  
S Fichelson ◽  
B Varet
Keyword(s):  
Bone Marrow ◽  
Myeloid Cells ◽  
Target Cells ◽  
Adherent Cells ◽  
Colony Stimulating Activity ◽  
Large Numbers ◽  
Bone Marrow Cultures ◽  
Nonadherent Cells ◽  
Marrow Cultures

Abstract The involvement of colony-stimulating activity (CSA) in murine long- term bone marrow cultures (LTBMC) was studied using bilayer agar cultures. The supernatants of LTBMC were removed, a layer of dense agar was spread over the cells adherent to the bottom of the flask, and fresh myeloid cells were plated as source of CFU-C in an upper agar layer. Large numbers of granulocytic and macrophagic colonies developed regularly when target cells were plated over adherent cells of nonrecharged and greater than 12 wk old LTBMC that were hematopoietically inactive (i.e., producing a low number of nonadherent cells). The removal of adherent cells from the myeloid cells used as source of CFU-C did not decrease the number of colonies. This suggests that adherent cells of LTBMC release CSA that is directly active on CFU- C. This CSA was no longer detectable over adherent layers of hematopoietically active LTBMC. A close inverse relationship was demonstrated between the number of nonadherent cells harvested before the assay and the level of CSA. No inhibitor for CSA was demonstrated in the supernatant of hematopoietically active cultures. Murine exogenous CSA incubated over the adherent layer host its activity within 24 hr, whereas in the same conditions human CSA retained its activity. These data demonstrate the production of CSA by the adherent layer of LTBMC and strongly suggest its specific in situ consumption by differentiating myeloid cells.

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