Regulation of I‐309 gene expression in human monocytes by endogenous interleukin‐1

Selvan, Rathinam S.; Zhou, Libo; Krangel, Michael S.

doi:10.1002/eji.1830270317

Cited by 39 publications

(30 citation statements)

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“…CCL1 has previously been reported to be produced from activated T lymphocytes, in particular Th1 effector cells, as well as IgG-and LPS-activated monocytes (35,36). However, our data would suggest that mast cells are the predominant cellular source of CCL1, expressing CCL1 mRNA at levels 100-fold higher than in T lymphocytes and monocytes in vitro.…”

Section: Discussioncontrasting

confidence: 71%

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Coordinated Involvement of Mast Cells and T Cells in Allergic Mucosal Inflammation: Critical Role of the CC Chemokine Ligand 1:CCR8 Axis

Gonzalo

Qiu

Lora

et al. 2007

The Journal of Immunology

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CCL1 is the predominant chemokine secreted from IgE-activated human and mouse mast cells in vitro, colocalizes to mast cells in lung biopsies, and is elevated in asthmatic airways. CCR8, the receptor for CCL1, is expressed by ∼70% of CD4+ T lymphocytes recruited to the asthmatic airways, and the number of CCR8-expressing cells is increased 3-fold in the airways of asthmatic subjects compared with normal volunteers. In vivo, CCL1 expression in the lung is reduced in mast cell-deficient mice after aeroallergen provocation. Neutralization of CCL1 or CCR8 deficiency results in reduced mucosal lung inflammation, airway hyperresponsiveness, and mucus hypersecretion to a similar degree as detected in mast cell-deficient mice. Adenoviral delivery of CCL1 to the lungs of mast cell-deficient mice restores airway hyperresponsiveness, lung inflammation, and mucus hypersecretion to the degree observed in wild-type mice. The consequences of CCR8 deficiency, including a marked reduction in Th2 cytokine levels, are comparable with those observed by depletion of CD4+ T lymphocytes. Thus, mast cell-derived CCL1- and CCR8-expressing CD4+ effector T lymphocytes play an essential role in orchestrating lung mucosal inflammatory responses.

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Section: Discussioncontrasting

confidence: 71%

“…Sections were hybridized with cRNA probes that were constructed from cDNA coding for CCR8 and CCL1 using standard method (29). Briefly, the probes were labeled with S 35 or digoxigen-UTA in the presence of SP6 and T7 polymerase. Following hybridization, the mRNA-cRNA signal was developed.…”

Section: Ccr8 and Ccl1 In Situ Hybridizationmentioning

confidence: 99%

Coordinated Involvement of Mast Cells and T Cells in Allergic Mucosal Inflammation: Critical Role of the CC Chemokine Ligand 1:CCR8 Axis

Gonzalo

Qiu

Lora

et al. 2007

The Journal of Immunology

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“…Their enhanced expression during inflammatory processes is stimulated by different cytokines in various cell types, i.e., by IL-1, TNF-␣, and IFN-␥ in human airway smooth-muscle cells (12), by IL-1 and IFN-␥ in both fibroblasts and epithelial cells (13) and by endogenous IL-1 in monocytes (14).…”

mentioning

confidence: 99%

Oncostatin M-Induced and Constitutive Activation of the JAK2/STAT5/CIS Pathway Suppresses CCL1, but Not CCL7 and CCL8, Chemokine Expression

Hintzen

Haan

Tuckermann

et al. 2008

The Journal of Immunology

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The recruitment of leukocytes to injured tissue is crucial for the initiation of inflammatory responses as well as for immune surveillance to fight tumor progression. In this study, we show that oncostatin M, a member of the IL-6-type cytokine family and potent proinflammatory cytokine stimulates the expression of the chemokines CCL1, CCL7, and CCL8 in primary human dermal fibroblasts at a faster kinetic than IL-1␤ or TNF-␣. The production of CCL1 and CCL8 is important for migration of monocytes, while specific Abs against CCL1 additionally inhibit the migration of T lymphocytes. We identify the mitogen-activated protein kinases ERK1/2 and p38 as crucial factors for the enhanced expression of CCL1 and CCL8. T he appropriate immune response relies on the interaction of various cell types orchestrated by direct cell contact or soluble factors. As an initial step, recruitment of leukocytes to sites of tissue damage or invaded pathogens occurs. This process is mainly controlled by members of the chemokine superfamily, in particular by the inducible "inflammatory" chemokines (1-3). This subfamily comprises the majority of the so far known 50 chemokines in humans and is distinguished from the constitutively expressed "homeostatic" chemokines. Apart from their function, chemokines can be sorted according to their structure into four groups, designated C, CX 3 C, CXC, and CC depending on the number and spacing of conserved cysteines (1-3). The family of monocyte-chemoattractant proteins (CCL2/MCP-1, CCL7/ MCP-3, CCL8/MCP-2, and CCL13/MCP-4) has mainly proinflammatory activities and exerts its biologic effects through binding to the G-protein coupled receptors CCR1 and CCR2, which are present on the cell surface of a variety of cell types (1, 3). CCL1/ I-309 has been originally identified as a gene expressed in activated T cell lines (4) and specifically binds to CCR8, which is expressed on the cell surface of polarized Th2 cells and regulatory T cells as well as macrophages (5-8).CCL1 as well as the MCP family members CCL7 and CCL8 are considered to play an important role in the recruitment of monocytes and T lymphocytes to sites of inflammation (9 -11). Their enhanced expression during inflammatory processes is stimulated by different cytokines in various cell types, i.e., by IL-1, TNF-␣, and IFN-␥ in human airway smooth-muscle cells (12), by IL-1 and IFN-␥ in both fibroblasts and epithelial cells (13) and by endogenous IL-1 in monocytes (14).In this study, we describe the regulation of CCL1, CCL7, and CCL8 by the IL-6-type cytokine oncostatin M (OSM) 3 in primary human dermal fibroblasts. OSM is a known proinflammatory cytokine, which is secreted by activated monocytes, neutrophils, and T lymphocytes (15). The human cytokine can signal through two receptor complexes: the type I receptor complex consisting of gp130, the common receptor subunit of all IL-6-type cytokines, and the LIF receptor or the type II receptor complex composed of gp130 and the OSM receptor ␤ subunit (16). In contrast, murine OSM only signals throu...

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“…Upon activation, CCL1 is produced by a number of cellular sources, including peripheral blood mononuclear cells, monocytes, activated T-lymphocytes and endothelial cells [8,13,14]. In vitro studies have shown that CCL1 as well as both CCL22/ monocyte-derived chemokine (MDC) and CCL17/ thymus-and activation-regulated chemokine (TARC) induce migration of lymphocytes, especially of the Th2 phenotype [13,14]. CCL22 and CCL17 activate these cells through the CC chemokine receptor (CCR)4, whereas CCL1 uses CCR8 [15,16].…”

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confidence: 99%

CC chemokine ligand 1 is released into the airways of atopic asthmatics

Montes-Vizuet¹

2006

European Respiratory Journal

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Regulation of I‐309 gene expression in human monocytes by endogenous interleukin‐1

Cited by 39 publications

References 39 publications

Coordinated Involvement of Mast Cells and T Cells in Allergic Mucosal Inflammation: Critical Role of the CC Chemokine Ligand 1:CCR8 Axis

Coordinated Involvement of Mast Cells and T Cells in Allergic Mucosal Inflammation: Critical Role of the CC Chemokine Ligand 1:CCR8 Axis

Oncostatin M-Induced and Constitutive Activation of the JAK2/STAT5/CIS Pathway Suppresses CCL1, but Not CCL7 and CCL8, Chemokine Expression

CC chemokine ligand 1 is released into the airways of atopic asthmatics

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