Marked increase in CC chemokine gene expression in both human and mouse mast cell transcriptomes following Fcepsilon receptor I cross-linking: an interspecies comparison

Nakajima, Toshiharu; Inagaki, Nobuya; Tanaka, Hiroyuki; Tanaka, Akane; Yoshikawa, Mamoru; Tamari, Mayumi; Hasegawa, Koichi; Matsumoto, Kenji; Tachimoto, Hiroshi; Ebisawa, Motohiro; Tsujimoto, Gozoh; Matsuda, Hiroshi; Nagai, Hiroichi; Saito, Hirohisa

doi:10.1182/blood-2002-02-0602

Cited by 104 publications

(75 citation statements)

References 48 publications

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“…13 In accordance with these results, we detected both IL-1R1 and IL-18Ra on mouse peritoneal mast cells by FACS analysis (data not shown). HUCBMCs express mRNA for IL-1R1 19 and, in the HUCBMCs we analyzed using DNA microarrays, levels of mRNA (mean7s.e.m. from 4-5 different batches of HUCBMCs) for IL-18Ra, IL-18Rb or T1/ST2 were 2.571.1% (n ¼ 5), 1.471.1% (n ¼ 4) or 1.770.3% (n ¼ 5), respectively, of levels of GAPDH mRNA in the same cells (Table 1).…”

Section: Resultsmentioning

confidence: 99%

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IL-33 can promote survival, adhesion and cytokine production in human mast cells

Iikura

Suto

Kajiwara

et al. 2007

Laboratory Investigation

349

310

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IL-33 is a recently identified member of the IL-1 family of molecules, which also includes IL-1 and IL-18. IL-33 binds to the receptor, T1/ST2/IL-1R4, and can promote cytokine secretion by Th2 cells and NF-kB phosphorylation in mouse mast cells. However, the effects of these molecules, especially IL-33, in human mast cells are poorly understood. Expression of the receptors for IL-1 family molecules, specifically, IL-1R1, IL-18R and T1/ST2, was detectable intracellularly in human umbilical cord blood-derived mast cells (HUCBMCs) by flow cytometry, but was scarcely detectable on the cells' surface. However, IL-1b, IL-18 or IL-33 induced phosphorylation of Erk, p38 and JNK in naïve HUCBMCs, and IL-33 or IL-1b, but not IL-18, enhanced the survival of naive HUCBMCs and promoted their adhesion to fibronectin. IL-33 or IL-1b also induced IL-8 and IL-13 production in naïve HUCBMCs, and enhanced production of these cytokines in IgE/anti-IgE-stimulated HUCBMCs, without enhancing secretion of either PGD 2 or histamine. Moreover, IL-33-mediated IL-8 production by HUCBMCs was markedly reduced by the p38 MAPK inhibitor, SB203580. In contrast to findings with mouse mast cells, IL-18 neither induced nor enhanced secretion of the mediators PGD 2 or histamine by HUCBMCs. Our findings identify previously unknown functions of IL-33 in human mast cells. One of these is that IL-33, like IL-1b, can induce cytokine production in human mast cells even in the absence of stimuli of FceRI aggregation. Our findings thus support the hypothesis that IL-33 may enhance mast cell function in allergic disorders and other settings, either in the presence or absence of co-stimulation of mast cells via IgE/antigen-FceRI signals.

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Section: Resultsmentioning

confidence: 99%

“…19 Assessment of gene expression levels and data analysis were performed as previously described. 19 …”

Section: Genechipmentioning

confidence: 99%

IL-33 can promote survival, adhesion and cytokine production in human mast cells

Iikura

Suto

Kajiwara

et al. 2007

Laboratory Investigation

349

310

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“…By confocal microscopy, we were able to colocalize CCL17 + cells and inflammatory cell ( Figure 6e) and endothelial ( Figure 6f) markers. We also measured the levels of three mast-cellspecific markers in the CNS of Ad-G/IL4-and Ad-Gtreated mice, as there are data indicating that CCL1 is mostly released by mast cells 18 and that mast cells are involved in CD4 + CD69 À CD25 + -regulatory T cells function. 19 No significant difference in mRNA of mast cell markers were observed between treated and control mice (Supplementary Figure 3).…”

Section: Il4 Gene Therapy Increases the Recruitment Of Treg Cells By mentioning

confidence: 99%

IL4 gene delivery to the CNS recruits regulatory T cells and induces clinical recovery in mouse models of multiple sclerosis

et al. 2008

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Central nervous system (CNS) delivery of anti-inflammatory cytokines, such as interleukin 4 (IL4), holds promise as treatment for multiple sclerosis (MS). We have previously shown that short-term herpes simplex virus type 1-mediated IL4 gene therapy is able to inhibit experimental autoimmune encephalomyelitis (EAE), an animal model of MS, in mice and non-human primates. Here, we show that a single administration of an IL4-expressing helper-dependent adenoviral vector (HD-Ad) into the cerebrospinal fluid (CSF) circulation of immunocompetent mice allows persistent transduction of neuroepithelial cells and long-term (up to 5 months) CNS transgene expression without toxicity.Mice affected by chronic and relapsing EAE display clinical and neurophysiological recovery from the disease once injected with the IL4-expressing HD-Ad vector. The therapeutic effect is due to the ability of IL4 to increase, in inflamed CNS areas, chemokines (CCL1, CCL17 and CCL22) capable of recruiting regulatory T cells (CD4 + CD69 À CD25 + Foxp3 + ) with suppressant functions. CSF delivery of HD-Ad vectors expressing anti-inflammatory molecules might represent a valuable therapeutic option for CNS inflammatory disorders.

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“…For example, purified populations of mast cells can present Ags to T cells by either MHC class I-or class II-restricted mechanisms in vitro (8 -11), and contact with activated T cells in vitro can induce some mast cell populations to secrete histamine, TNF, and metalloproteinase 9 and to exhibit enhanced levels of IL-4 mRNA (12)(13)(14)(15). Besides representing a major potential source of TNF (16,17), which can have several effects that influence T cell recruitment, activation, and function (18 -21), at least some mast cells can produce many other factors, including CCL2, CCL3, CCL4, CCL5, XCL1, IL-16, and leukotriene B 4 , which also have the potential to enhance T cell recruitment to local inflammatory sites (5,(22)(23)(24)(25).…”

Section: Ast Cells Represent Important Effector Cells In Th2-andmentioning

confidence: 99%

Mast Cells Enhance T Cell Activation: Importance of Mast Cell Costimulatory Molecules and Secreted TNF

Nakae

Suto

Iikura

et al. 2006

The Journal of Immunology

356

306

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We recently reported that mast cells stimulated via FcεRI aggregation can enhance T cell activation by a TNF-dependent mechanism. However, the molecular mechanisms responsible for such IgE-, Ag- (Ag-), and mast cell-dependent enhancement of T cell activation remain unknown. In this study we showed that mouse bone marrow-derived cultured mast cells express various costimulatory molecules, including members of the B7 family (ICOS ligand (ICOSL), PD-L1, and PD-L2) and the TNF/TNFR families (OX40 ligand (OX40L), CD153, Fas, 4-1BB, and glucocorticoid-induced TNFR). ICOSL, PD-L1, PD-L2, and OX40L also are expressed on APCs such as dendritic cells and can modulate T cell function. We found that IgE- and Ag-dependent mast cell enhancement of T cell activation required secreted TNF; that TNF can increase the surface expression of OX40, ICOS, PD-1, and other costimulatory molecules on CD3+ T cells; and that a neutralizing Ab to OX40L, but not neutralizing Abs to ICOSL or PD-L1, significantly reduced IgE/Ag-dependent mast cell-mediated enhancement of T cell activation. These results indicate that the secretion of soluble TNF and direct cell-cell interactions between mast cell OX40L and T cell OX40 contribute to the ability of IgE- and Ag-stimulated mouse mast cells to enhance T cell activation.

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Marked increase in CC chemokine gene expression in both human and mouse mast cell transcriptomes following Fcepsilon receptor I cross-linking: an interspecies comparison

Cited by 104 publications

References 48 publications

IL-33 can promote survival, adhesion and cytokine production in human mast cells

IL-33 can promote survival, adhesion and cytokine production in human mast cells

IL4 gene delivery to the CNS recruits regulatory T cells and induces clinical recovery in mouse models of multiple sclerosis

Mast Cells Enhance T Cell Activation: Importance of Mast Cell Costimulatory Molecules and Secreted TNF

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