Differential expression of cytokines in human blood monocyte subpopulations [see comments]

Ziegler‐Heitbrock, H. W. L.; Ströbel, M; Kieper, D; Fingerle, G; Schlunck, T; Petersmann, I; Ellwart, Joachim W.; Blumenstein, M; Haas, Jürgen

doi:10.1182/blood.v79.2.503.503

Cited by 92 publications

(23 citation statements)

References 41 publications

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“…There is also a subset of peripheral blood monocytes that expresses CD14 less intensely, but with an increased expression of CD16 on the cell membrane (CD14 + CD16 + ). 32,33 This subset also seems to be distinct from regular blood monocytes, since they produce less TNF, IL-1b and IL-6 34 and may represent an early stage of differentiation towards alveolar macrophages. Another possibility is that GM-CSF promotes differentiation of monocytes towards antigen-presenting cells.…”

Section: Discussionmentioning

confidence: 98%

Granulocyte–macropha ge colony‐stimulating factor down‐regulates CD14 expression on monocytes

Kruger

Winkel²,

Wit³

et al. 1996

Immunology

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SUMMARYCD14 is a differentiation-stage-linked glycosyl-phophatidyl-inositol-linked glycoprotein on human peripheral blood monocytes and tissue macrophages, which functions as a receptor for lipopolysaccharide. Here, the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine with proliferation-and differentiation-inducing properties on myeloid lineage cells, were studied on CD14 expression by peripheral blood cells. GM-CSF down-regulated the membrane expression of CD14 on monocytes, while it up-regulated expression on neutrophils. GM-CSF also decreased the spontaneous release of CD14 in monocyte culture supernatants. Down-regulation of CD14 expression and release was accompanied by a decrease in the mRNA transcript for CD14, suggesting that it most likely reflects an effect on the transcriptional level. The functional significance of this phenomenon, and its potential relation to the terminal differentiation of monocytes, are discussed.

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Section: Discussionmentioning

confidence: 98%

Granulocyte–macropha ge colony‐stimulating factor down‐regulates CD14 expression on monocytes

Kruger

Winkel²,

Wit³

et al. 1996

Immunology

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“…Yet, we provide new evidence for a functional immaturity of monocytes at this stage. High expression of CD16 on monocytes has been shown to correlate with increased clearance of pathogens at the site of infection [11][12][13]15], which may help compensate for the lack of IL-1β in the early neonatal period. On the other hand, the lack of LPS-mediated pro-IL-1β response in CD14 low monocytes potentially represents an early developmental stage at which monocyte IL-1β responses are dispensable.…”

Section: Discussionmentioning

confidence: 99%

“…These CD14 high /CD16 neg monocytes make up the majority of monocytes in peripheral adult blood, and have been proposed to be capable of producing high amounts of IL-10 [11]. In contrast, the smaller, nonclassical CD14 low /CD16 pos monocytes express high levels of the antigenpresenting molecule HLA-DR [12], as well as cytokine TNF-α [13]. This latter subset has been proposed to play an important immediate responder "proinflammatory" role in sepsis [11,14,15].…”

Section: Introductionmentioning

confidence: 99%

Impaired NLRP3 inflammasome activity during fetal development regulates IL‐1β production in human monocytes

et al. 2014

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Interleukin-1β (IL-1β) production is impaired in cord blood monocytes. However, the mechanism underlying this developmental attenuation remains unclear. Here, we analyzed the extent of variability within the Toll-like receptor (TLR)/NLRP3 inflammasome pathways in human neonates. We show that immature low CD14 expressing/CD16 pos monocytes predominate before 33 weeks of gestation, and that these cells lack production of the pro-IL-1β precursor protein upon LPS stimulation. In contrast, high levels of pro-IL-1β are produced within high CD14 expressing monocytes, although these cells are unable to secrete mature IL-1β. The lack of secreted IL-1β in these monocytes parallels a reduction of NLRP3 induction following TLR stimulation resulting in a lack of caspase-1 activity before 29 weeks of gestation, whereas expression of the apoptosisassociated speck-like protein containing a CARD and function of the P2×7 receptor are preserved. Our analyses also reveal a strong inhibitory effect of placental infection on LPS/ATP-induced caspase-1 activity in cord blood monocytes. Lastly, secretion of IL-1β in preterm neonates is restored to adult levels during the neonatal period, indicating rapid maturation of these responses after birth. Collectively, our data highlight important developmental mechanisms regulating IL-1β responses early in gestation, in part due to a downregulation of TLR-mediated NLRP3 expression. Such mechanisms may serve to limit potentially damaging inflammatory responses in a developing fetus.Keywords: Human r Inflammasome r Interleukin-1 beta (IL-1β) r Neonate r Toll-like receptor Additional supporting information may be found in the online version of this article at the publisher's web-site Correspondence: Dr. Pascal M. Lavoie e-mail: plavoie@cw.bc.ca * These authors contributed equally to this work.C 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu Eur. J. Immunol. 2015. 45: 238-249 Innate immunity 239 IntroductionNewborns are at high risk of infections, in part due to attenuated innate immune defenses [1]. The cytokine interleukin-1β (IL-1β) is an important inflammatory mediator in response to infections [2]. Mice lacking IL-1β display impaired acute phase and pyrogenic responses [3], and increased susceptibility to pathogens commonly encountered in the neonatal period [4,5]. In contrast, high levels of IL-1β in a fetus can result in autoimmune organ damage [2], as well as lethal metabolic disturbances including severe weight loss and hypoglycemia [6]. Together, these data illustrate the evolutionary importance of a tight regulation of IL-1β in order to avoid inflammation-mediated organ damage, neurological injury [7], or even premature birth in a developing human [2,8].Monocytes are primarily responsible for the production of IL-1β in circulating blood [9,10]. Three subsets predominate in humans: "Classical" monocytes express CD14, but lack expression of the immunoglobulin receptor CD16. These CD14 high /CD16 neg monocytes make up the majority of monocytes in peripheral adult bloo...

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“…Of particular interest in the context of phenotype-function relations, Ziegler-Heitbrock el al. showed that the small subset of normal monocytes co-expressing CD 14 dimly and CD 16 brightly have a lower phagocytic capacity and a lower stimulated cytokine production [43], On the other hand, Capsoni et al showed a decreased antibody-mediated phagocytosis by monocytes from AIDS patients, despite an increased density of FC7RI, an increased proportional expression of FC7RIII, and elevated levels of IFN-7 [44].…”

Section: Co-expression Of CD 14 Fcyri and Cdllb But Not Fey Riiimentioning

confidence: 99%

Expression patterns of Fcγ receptors, HLA-DR and selected adhesion molecules on monocytes from normal and HIV-infected individuals

Locher

Vanham

Kestens

et al. 1994

Clinical and Experimental Immunology

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SUMMARY The expression and co‐expression profiles of functionally important monocyte surface markers were compared between control and HIV+ individuals using combined physical gating and dim CD4 expression to delineate the monocytes. The FcγRII (CD32), the MHC class II antigen HLADR and the adhesion molecules CDIIa (LFA‐1α), CD18 and CD54 (ICAM‐1) showed an unimodal distribution. Of these markers, CDI Ia and HLA‐DR were up‐regulated in the HIV+ subjects compared with controls. The expression levels of the adhesion molecules correlated with each other in both patients and controls. The CD11b (CR3‐α), CD14, FcγRI, and FcγRIII markers were bimodally distributed. Compared with controls, monocytes from seropositives contained fewer CDbright+ cells, an equal proportion of FcγIbright+ cells, but twice as many FCγ RIII+ cells. The expression level of FcγRI and CD11b within their brightly positive subset increased as CD4T cells decreased. Both in patients and controls, co‐expression of bright CD11b, CD14 and FCγRI was shown, whereas the FcγRIII+ cells were negative or dim positive for the former triad. We conclude that the expression of two FcγR (I and III), of the adhesion molecules CD11a and CD11b and of HLA‐DR showed particular alterations on monocytes from HIV+ subjects. The relationship of these phenotypic observations with altered cytokine profiles and altered monocyte function is discussed.

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Differential expression of cytokines in human blood monocyte subpopulations [see comments]

Cited by 92 publications

References 41 publications

Granulocyte–macropha ge colony‐stimulating factor down‐regulates CD14 expression on monocytes

Granulocyte–macropha ge colony‐stimulating factor down‐regulates CD14 expression on monocytes

Impaired NLRP3 inflammasome activity during fetal development regulates IL‐1β production in human monocytes

Expression patterns of Fcγ receptors, HLA-DR and selected adhesion molecules on monocytes from normal and HIV-infected individuals

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