Synergism of glucocorticoids with granulocyte macrophage colony stimulating factor (GM-CSF) but not interferon gamma (IFN-γ) or interleukin-4 (IL-4) on induction of HLA class II expression on human monocytes

Sadeghi, Roya; Hawrylowicz, Catherine M.; Chernajovsky, Yuti; Feldmann, Marc

doi:10.1016/1043-4666(92)90069-4

Cited by 20 publications

(15 citation statements)

References 40 publications

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“…The significant increase in MHC class-I1 surface antigen expressions that we detected in the patients treated with rhGM-CSF agrees with previous in vitro studies (2,21,22). The increase in HLA surface molecules on monocytes seems to be induced directly by GM-CSF via a mechanism that differs from indirect mediation through IFN-y secretion (22). GM-CSF is also known to induce rapid up-regulation of neutrophil and monocyte surface CD1 l b (4,7,24).…”

Section: Discussionsupporting

confidence: 81%

“…The significant decrease in CD 14 expression on CD14b"phfCD16-cells that we found in the patients treated with rhGM-CSF in vivo correlates well with the reported down-modulation of expression levels of the myeloid glycoprotein CD14 in cultures of freshly isolated, normal, peripheral blood monocytes by GM-CSF (10). The significant increase in MHC class-I1 surface antigen expressions that we detected in the patients treated with rhGM-CSF agrees with previous in vitro studies (2,21,22). The increase in HLA surface molecules on monocytes seems to be induced directly by GM-CSF via a mechanism that differs from indirect mediation through IFN-y secretion (22).…”

Section: Discussionsupporting

confidence: 81%

“…Our in vivo data also differ from data from in vitro studies on purified normal human monocytes cultured with M-CSF that did not show induction of higher expression levels of DR surface antigens (22). These discrepant results on in vitro-cultured, separated monocytes may be related to the absence of human plasma that can contain factors that affect in vivo biological responses of cells.…”

Section: Discussioncontrasting

confidence: 57%

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Alterations in phenotype and cell‐surface antigen expression levels of human monocytes: Differential response to in vivo administration of rhm‐csf or rhgm‐csf

et al. 1995

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We investigated, via multicolor flow cytometry, the in vivo effects of colony-stimulating factors (CSFs) on cell size, frequencies, and expression of surface antigens on peripheral blood monocytes from melanoma patients treated concurrently with CSFs and tumor-specific monoclonal antibody (mAb) R24. Recombinant human macrophage colony-stimulating factor (rhM-CSF) increased cell size, relative percentages of monocytes, percentages of CD14+, HLA-DQ+, C D l l b+, and CD16+ monocytes, and cell-surface expressions of HLA-DR and C D l l b; rhM-CSF also up-regulated cell-surface expression of CD14 on CD14brigh'CD16-monocytes. Recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) increased cell size, percentages of CD14+, HLA-DQ+, and C D l l b+ monocytes, and cell-surface expressions of HLA-DR, HLA-DQ, C D l l b, and CD58. Relative percentages of monocytes and CD16+ cells and cell-surface expression of CD14 on CD14brightCD1 6-monocytes decreased. In addition, monocytes derived from patients treated with rhM-CSF showed functional activity when assayed in vitro for antibody-dependent cellular cytotoxicity (ADCC). During treatment and coincident with increased CD16 expression, monocytes derived from rhM-CSF patients had enhanced levels of cytotoxicity towards melanoma target cells compared to healthy controls and to patients treated with rhGM-CSF. o 1995 Wiley-Liss, Inc.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionsupporting

confidence: 81%

Section: Discussioncontrasting

confidence: 57%

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Alterations in phenotype and cell‐surface antigen expression levels of human monocytes: Differential response to in vivo administration of rhm‐csf or rhgm‐csf

et al. 1995

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“…Glucocorticoids inhibit a variety of macrophage inflammatory responses. In particular, Dex has been shown to inhibit macrophage activation by IFN-␥ in terms of nitric oxide production and upregulation of MHC class II expression (37,38), although not all studies concur that Dex can inhibit IFN-␥-induced upregulation of MHC class II expression (39,40). We confirmed the ability of Dex to inhibit IFN-␥-induced nitric oxide via suppression of iNOS gene transcription, although we did not observe any effect of Dex on IFN-␥-induced upregulation of RT1B␣ gene expression.…”

Section: Discussionmentioning

confidence: 99%

Interferon-γ Augments Acute Macrophage-Mediated Renal Injury Via a Glucocorticoid-Sensitive Mechanism

Ikezumi¹,

Atkins²,

Nikolic-Paterson³

2003

Journal of the American Society of Nephrology

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Abstract. Macrophages have been implicated in causing renal injury in both human and experimental kidney disease. The aim of the current study was to determine whether modulating the state of macrophage activation directly affects the capacity of these cells to cause renal injury. This was investigated using an adoptive transfer model in which macrophage activation can be manipulated in vitro, using interferon-␥ (IFN-␥) or dexamethasone (Dex), and then macrophage-mediated renal injury determined in vivo. In this model, rats were made leukopenic by administration of cyclophosphamide (CyPh). Two days later (day 0), animals were injected with sheep anti-GBM serum followed by a single injection of rat NR8383 macrophages on day 1 and then killed 3 or 24 h after cell transfer. NR8383 macrophages were incubated IFN-␥ and/or Dex before adoptive transfer into animals. Induction of proteinuria and glomerular cell proliferation (PCNAϩ cells) in this model was dependent on transfer of NR8383 macrophages. Exposure of macrophages to IFN-␥ for 18 h (but not 3 h) before transfer caused a twofold increase in the degree of proteinuria and glomerular cell proliferation compared with unstimulated cells

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“…The ability of glucocorticoids to induce both positive and negative selection in the thymic micro-environment provides evidence that the bimodal regulatory capacity of glucocorticoids proposed by Munck is operant physiologically. In certain conditions, glucocorticoids enhance proinflammatory phenomena in vitro, such as T cell proliferation [27] and cytokine-stimulated MHC class II expression [28]. As an example in vivo, hypophysectomised rats, which lack circulating pituitary hormones and therefore a stressresponsive adrenal gland, are resistant to the induction of adjuvant arthritis [29].…”

mentioning

confidence: 99%

Glucocorticoid regulation of inflammation: The plot thickens

Morand

Leech

1999

Inflammation Research

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While glucocorticoids are widely used in the suppression of immune-inflammatory diseases, much remains unknown about the contribution of endogenous adrenal glucocorticoids to inflammatory regulation. It is now well understood that glucocorticoids are increased by inflammatory stress and provide for responsive limitation of inflammation. It is self-evident that the immune response in healthy animals takes place in a milieu characterised by background levels of glucocorticoids. It is less well appreciated, however, that basal levels of glucocorticoids may in fact be a requirement for a normal immune response. In fact, extensive data exist supporting the hypothesis that glucocorticoids interact with the immune-inflammatory system in a biphasic, concentration dependent fashion. No mechanistic explanation for this apparent paradox has previously existed. Recently, the cytokine macrophage migration inhibitory factor (MIF), while possessing pleiotropic pro-inflammatory properties, has been demonstrated to be glucocorticoid-inducible. This observation has the potential to explain key aspects of the biphasic regulation of inflammatory response by endogenous glucocorticoids.

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Synergism of glucocorticoids with granulocyte macrophage colony stimulating factor (GM-CSF) but not interferon gamma (IFN-γ) or interleukin-4 (IL-4) on induction of HLA class II expression on human monocytes

Cited by 20 publications

References 40 publications

Alterations in phenotype and cell‐surface antigen expression levels of human monocytes: Differential response to in vivo administration of rhm‐csf or rhgm‐csf

Alterations in phenotype and cell‐surface antigen expression levels of human monocytes: Differential response to in vivo administration of rhm‐csf or rhgm‐csf

Interferon-γ Augments Acute Macrophage-Mediated Renal Injury Via a Glucocorticoid-Sensitive Mechanism

Glucocorticoid regulation of inflammation: The plot thickens

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