Production of colony-stimulating factor 1 by T cells: Possible involvement in their interaction with antigen-presenting cells

Zisman, Einat; Waisman, Ari; Ben-Yair, Edith; Tartakovsky, Boris

doi:10.1016/1043-4666(93)90062-a

Cited by 9 publications

(8 citation statements)

References 42 publications

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“…Although little is known about the biology of hCSF-1, and relatively little is known about mouse CSF-1 outside of its role as a macrophage growth and differentiation factor, there are some studies that clearly suggest a role for hCSF-1 in modulating the innate and cellmediated immune responses. The expression of hCSF-1 on the surface of activated, but not resting, human T cells, as indicated by our expression cloning experiments, is consistent with other reports (19,49,57,59). Zisman et al (59) performed proliferation assays using antigen-specific human T-cell clones, irradiated syngeneic spleen cells, and antigen and found that the inclusion of hCSF-1 blocking antibodies inhibited T-cell proliferation.…”

Section: Discussionsupporting

confidence: 91%

“…CSF-1 is a cytokine that traditionally has been considered a macrophage growth and differentiation factor, owing in large part to work performed in the mouse system (47). Remarkably little is known about the biological activity of hCSF-1; however, its expression by fibroblasts, endothelial cells, monocytes/macrophages (reference 41 and references therein), and activated human T cells and T-cell lines (25,59) as well as the expression of the CSF-1 receptor (CSF-1R) on osteoclasts and on myeloid, epithelial, and B cells strongly suggest that hCSF-1 is a pleiotropic cytokine with many as yet undetermined activities.…”

Section: Resultsmentioning

confidence: 99%

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The Epstein-Barr Virus BARF1 Gene Encodes a Novel, Soluble Colony-Stimulating Factor-1 Receptor

Strockbine

Cohen

Farrah

et al. 1998

J Virol

133

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Epstein-Barr virus (EBV) is a ubiquitous herpesvirus associated with infectious mononucleosis and several tumors. The BARF1 gene is transcribed early after EBV infection from the BamHI A fragment of the EBV genome. Evidence shown here indicates that the BARF1 protein is secreted into the medium of transfected cells and from EBV-carrying B cells induced to allow lytic replication of the virus. Expression cloning identified colony-stimulating factor-1 (CSF-1) as a ligand for BARF1. Computer-assisted analyses indicated that subtle amino acid sequence homology exists between BARF1 and c-fms, the cellular proto-oncogene that is the receptor for CSF-1. Recombinant BARF1 protein was found to be biologically active, and it neutralized the proliferative effects of human CSF-1 in a dose-dependent fashion when assayed in vitro. Since CSF-1 is a pleiotropic cytokine best known for its differentiating effects on macrophages, these data suggest that BARF1 may function to modulate the host immune response to EBV infection.

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Section: Discussionsupporting

confidence: 91%

Section: Resultsmentioning

confidence: 99%

The Epstein-Barr Virus BARF1 Gene Encodes a Novel, Soluble Colony-Stimulating Factor-1 Receptor

Strockbine

Cohen

Farrah

et al. 1998

J Virol

133

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“…Although the ability of activated T cells to produce M‐CSF messenger RNA (mRNA) and to express the membrane bound form of M‐CSF has been reported previously,( 25,26 ) here, for the first time, we show that activated T cells also produce large concentrations of the soluble form of M‐CSF. Interestingly, despite previous reports that M‐CSF is an important cofactor for RANKL activity,( 12,13 ) our data show that complete neutralization of M‐CSF by anti‐M‐CSF antibody failed to impact OC survival or block OC formation in this culture system.…”

Section: Discussionsupporting

confidence: 43%

T Cell Activation Induces Human Osteoclast Formation via Receptor Activator of Nuclear Factor κB Ligand-Dependent and -Independent Mechanisms

Weitzmann

Cenci

Rifas

et al. 2001

Journal of Bone and Mineral Research

150

110

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In unstimulated conditions, osteoclast (OC) formation is regulated by stromal cell production of the key osteoclastogenic factors receptor activator of nuclear factor B ligand (RANKL) and macrophage colonystimulating factor (M-CSF). However, the mechanisms of accelerated osteoclastogenesis and bone loss characteristic of inflammatory conditions are poorly understood but appear to involve T cells. In addition, the mechanism by which OCs arise spontaneously in cultures of peripheral blood mononuclear cells in the absence of stromal cells or added cytokines remains unclear. Using a stromal cell free human osteoclast generating system, we investigated the ability of activated T cells to support osteoclastogenesis. We show that when activated by phytohemagglutinin-P (PHA), T cells (both CD4؉ and CD8 ؉ ) stimulate human OC formation in vitro. Although both soluble M-CSF and RANKL were detected in activated T cell supernatants, the presence of M-CSF was not essential for macrophage survival or RANKL-dependent osteoclast formation, suggesting that other soluble T cell-derived factors were capable of substituting for this cytokine. We also found that saturating concentrations of osteoprotegerin (OPG) failed to neutralize 30% of the observed OC formation and that T cell conditioned medium (

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“…Several early publications described Csf1 expression in cultured CD4 + T cells stimulated extensively in vitro [44–47]. In addition, one study has reported detection of lymphocyte-associated MCSF in human lymph node tumor biopsies [48], and two others found evidence for Csf1 production in decidual T cells during pregnancy [49,50].…”

Section: Resultsmentioning

confidence: 99%

Macrophage Colony Stimulating Factor Derived from CD4+ T Cells Contributes to Control of a Blood-Borne Infection

et al. 2016

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Dynamic regulation of leukocyte population size and activation state is crucial for an effective immune response. In malaria, Plasmodium parasites elicit robust host expansion of macrophages and monocytes, but the underlying mechanisms remain unclear. Here we show that myeloid expansion during P. chabaudi infection is dependent upon both CD4+ T cells and the cytokine Macrophage Colony Stimulating Factor (MCSF). Single-cell RNA-Seq analysis on antigen-experienced T cells revealed robust expression of Csf1, the gene encoding MCSF, in a sub-population of CD4+ T cells with distinct transcriptional and surface phenotypes. Selective deletion of Csf1 in CD4+ cells during P. chabaudi infection diminished proliferation and activation of certain myeloid subsets, most notably lymph node-resident CD169+ macrophages, and resulted in increased parasite burden and impaired recovery of infected mice. Depletion of CD169+ macrophages during infection also led to increased parasitemia and significant host mortality, confirming a previously unappreciated role for these cells in control of P. chabaudi. This work establishes the CD4+ T cell as a physiologically relevant source of MCSF in vivo; probes the complexity of the CD4+ T cell response during type 1 infection; and delineates a novel mechanism by which T helper cells regulate myeloid cells to limit growth of a blood-borne intracellular pathogen.

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Production of colony-stimulating factor 1 by T cells: Possible involvement in their interaction with antigen-presenting cells

Cited by 9 publications

References 42 publications

The Epstein-Barr Virus BARF1 Gene Encodes a Novel, Soluble Colony-Stimulating Factor-1 Receptor

The Epstein-Barr Virus BARF1 Gene Encodes a Novel, Soluble Colony-Stimulating Factor-1 Receptor

T Cell Activation Induces Human Osteoclast Formation via Receptor Activator of Nuclear Factor κB Ligand-Dependent and -Independent Mechanisms

Macrophage Colony Stimulating Factor Derived from CD4+ T Cells Contributes to Control of a Blood-Borne Infection

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