Monocyte-derived dendritic cells represent a transient stage of differentiation in the myeloid lineage

Häusser, G; Ludewig, Burkhard; Gelderblom, Hans R.; Tsunetsugu-Yokota, Yasuko; Akagawa, Kiyoko S.; Meyerhans, Andreas

doi:10.1016/s0171-2985(97)80085-x

Cited by 48 publications

(33 citation statements)

References 24 publications

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“…However, if the macrophages are washed after cytokine treatment and held in the absence of cytokine for 1-2 days before LPS stimulation, the functional response pattern is essentially identical to that of macrophages that had not been treated with cytokine. A similar reversion to basal macrophage phenotype is observed when human monocyte-derived, immature dendritic cells (DC) are removed from IL-4 + granulocyte macrophage-colony stimulating factor (GM-CSF) and placed in a neutral environment [20]. We have been able to corroborate this observation with immature DC (CD11c+) derived by IL-4 + GM-CSF treatment of murine BM-derived and peritoneal macrophages (unpublished data).…”

Section: Functional Heterogeneity Of Macrophages Is a Results Of Diffesupporting

confidence: 58%

Functional plasticity of macrophages: reversible adaptation to changing microenvironments

Stout

Suttles

2004

Journal of Leukocyte Biology

655

554

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There has been substantial research activity in the past decade directed at phenotyping macrophage lineages and defining macrophage functional subsets or patterns of activity. The emphasis over the past 2-3 years has been to divide macrophage functional patterns into type 1 (Th1-driven) or type 2 (Th2-driven) functions. However, a huge array of environmental factors (including cytokines, chemokines, pattern recognition receptors, hormones) differentially regulates macrophage response patterns, resulting in the display of numerous distinct, functional phenotypes. Upon stimulation, a macrophage does not display just a single set of functions but rather displays a progression of functional changes in response to the progressive changes in its microenvironment. The remarkable ability of monocytes and tissue macrophages to adapt to changes in their microenvironment challenges the thesis that macrophages displaying unique tissue-specific or response-specific, functional patterns represent distinct lineages. With the exception of mature osteoclasts and mature dendritic cells, evidence supporting stable differentiation as the basis for macrophage functional heterogeneity is equivocal. The concept of whether macrophages develop into functional subsets as opposed to continuously adapting their functional pattern in response to the changing environment of a progressive inflammatory response is important to resolve from the perspectives of therapeutic targeting and understanding the role of macrophages in disease pathogenesis.

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Section: Functional Heterogeneity Of Macrophages Is a Results Of Diffesupporting

confidence: 58%

Functional plasticity of macrophages: reversible adaptation to changing microenvironments

Stout

Suttles

2004

Journal of Leukocyte Biology

655

554

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“…These diverse and somewhat contradictory findings may reflect the plasticity of the target cells. Cells of the mononuclear phagocyte lineage can proceed from being undifferentiated immature monocytes to widely diverse forms, including dendritic cells (9,25), in vivo and in vitro, depending on the environmental stimuli encountered. Adherence of the cells to different surfaces and exposure to different cytokines prior to apoptosis may have resulted in biochemically and functionally different cells in the different studies.…”

Section: Discussionmentioning

confidence: 99%

Identification and Characterization of Murine Cytotoxic T Cells That KillMycobacterium tuberculosis

Silva

Lowrie

2000

Infect Immun

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As we seek to develop and evaluate new vaccines against tuberculosis, it is desirable that we understand the mechanisms of protective immunity in our models. Adoptive transfer of protection with hsp65-specific T-cell clones from infected or vaccinated mice into naïve mice had indicated that cytotoxic T cells can make a major contribution to protection. We characterized 28 CD4 ؉ CD8 ؊ and 28 CD4 ؊ CD8 ؉ hsp65-specific T-cell clones derived from infected or vaccinated mice. Half of the CD4 ؉ CD8 ؊ and 64% of the CD4 ؊ CD8 ؉ clones were cytotoxic. Cytotoxicity was associated with high expression of CD44 and gamma interferon production. Most (86%) of the cytotoxic CD4 ؉ CD8 ؊ clones lysed target cells via the Fas-FasL pathway, and most (83%) of the cytotoxic CD4 ؊ CD8 ؉ clones lysed target cells via cytotoxic granules. Only the clones using the granulemediated pathway caused substantial loss of viability of virulent Mycobacterium tuberculosis during lysis of infected macrophages, and the degree of killing closely correlated with the availability of granule marker enzyme activity. Granule-mediated cytotoxicity thus may have a key role in protection against tuberculosis by delivering mycobactericidal granule contents.New vaccines are needed in the fight against tuberculosis (1), but the designing and testing of new vaccines is hampered by our poor understanding of the mechanisms of acquired protective immunity. It is not simply that the key protective antigens have yet to be identified (15); we do not know with certainty what kinds of responses are needed. This knowledge would help both to design vaccines for the best balance of responses and to design clinical tests to monitor or predict vaccine efficacy in the field.Traditionally, protection against tuberculosis has been regarded as due to phagocytosis and killing of Mycobacterium tuberculosis by immunologically activated macrophages and monocytes (12). This is a result of a type 1 cellular response in which gamma interferon (IFN-␥) is produced by antigen-specific T lymphocytes, as distinct from a type 2 response, in which the cells produce interleukin (IL-4) (19). IFN-␥ is the main macrophage-activating factor, and it has been shown to be essential for protection (5,8). However, substantial killing by the activated macrophages or monocytes has been difficult to demonstrate in vitro (4,16,18,24), and there is increasing evidence for a protective role for antigen-specific cytotoxic T lymphocytes, in both murine and human tuberculoses (2, 17, 22). It is not clear how these cells are protective. One possibility is that the cytotoxic T cells are needed to release bacteria from safe havens inside ineffective macrophages so that they can be phagocytosed by fresh, fully activated monocytes or macrophages (7). Alternatively, studies with human peripheral blood cells in vitro have indicated that lysis of infected macrophages by antigen-specific T cells can directly result in death of the bacteria (17, 22). Mycobacterial death can be due to toxic enzymes discharged from lymph...

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“…One of these lineage progressions leads to formation of myeloid progenitor cells that in turn can differentiate into monocytes. Monocytes are a highly plastic cell type that can differentiate into dendritic cells, various types of tissue macrophages, and Kupffer cells (Wisse, 1974;Eiermann et al, 1989;Hausser et al, 1997;Randolph et al, 1998).…”

Section: Origin Of Circulating Endothelial Cell Progenitorsmentioning

confidence: 99%

“…CD14 ϩ cells cultured in the presence of oncostatin M and interleukin-4 form a homogeneous population lacking dendritic or macrophage antigens and upregulate VE-cadherin and begin to express CD34 (Fernandez Pujol et al, 2001). In addition, although its role in adult endothelial cell progenitor differentiation has not been tested directly, M-CSF appears to play a role in directing dendritic cells into a more endothelial cell-like phenotype (Hausser et al, 1997). Moreover, in the embryo M-CSF is critical for endothelial cell differentiation in the aorta/gonad/mesenephros region (Minehata et al, 2002).…”

Section: Molecular Regulation Of Endothelial Cell Progenitorsmentioning

confidence: 99%

Hemangioblasts, angioblasts, and adult endothelial cell progenitors

Schatteman

Awad

2003

Anat. Rec.

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After decades of speculation, proof of embryonic hemangioblasts finally emerged a few years ago. Surprisingly, at about the same time, evidence for adult hemangioblasts began to appear, and recent single-cell bone marrow transplants have confirmed their existence. Embryonic and adult hemangioblasts appear to share antigenic determinants, including CD34, ACC133, and VEGFR2, although their phenotype may be plastic. They also respond to similar factors, prominent among them vascular endothelial growth factor (VEGF). In the adult, hemangioblasts reside principally in the bone marrow, although they may subsequently leave that niche to reside in nonhematopoietic tissues. A number of studies indicate that these cells or their progeny may be a significant source of endothelial cells in adult pathologic and nonpathologic vascularization, and may participate in vascular repair. In addition to hemangioblasts, a more differentiated source of endothelial cell progenitors may be present in the blood, namely, monocytes or monocytic-like cells. The relative importance of the two cell types in vivo is not clear, though endothelial cells derived from the two sources may not be identical, and hemangioblasts seem to provide a stimulus for differentiation of the monocytes. Treatment with exogenous bone marrow-derived cells can promote neovascularization, accelerate restoration of blood flow to ischemic tissues, and improve cardiac function after infarct. Hence, there is great hope that either alone, in combination with angiogenic factors, or as gene therapy vectors, we can harness these cells to treat ischemic and vascular diseases in the relatively near future. Anat Rec Part A 276A: 13-21, 2004.

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Monocyte-derived dendritic cells represent a transient stage of differentiation in the myeloid lineage

Cited by 48 publications

References 24 publications

Functional plasticity of macrophages: reversible adaptation to changing microenvironments

Functional plasticity of macrophages: reversible adaptation to changing microenvironments

Identification and Characterization of Murine Cytotoxic T Cells That KillMycobacterium tuberculosis

Hemangioblasts, angioblasts, and adult endothelial cell progenitors

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