Regulation of the class II and class I MHC pathways in human THP-1 monocytic cells by interleukin-27

Feng, Xiao; Liu, Na; Yang, Shangda; Hu, Li Yan; Chen, Xiao Li; Fang, Zhi; Ren, Qian; Lu, Shi Hong; Liu, Bin; Han, Zhongchao

doi:10.1016/j.bbrc.2007.12.154

Cited by 37 publications

(39 citation statements)

References 18 publications

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“…IL-27 was recently shown to upregulate MHC molecules in several cell subsets (Feng et al 2007;Feng et al 2008;Kamiya et al 2004;Salcedo et al 2004). CIITA is a critical transcriptional activator that coordinately regulates the expression of the majority of genes involved in antigen processing and presentation.…”

Section: Il-27 Modulates Antigen Presentationmentioning

confidence: 99%

“…IL-27 thus not only induces HLA I heavy-chain expression, but also induces genes involved in antigen processing and the assembly of MHC class I molecules (Feng et al 2008). Salcedo et al found four to fivefold upregulation of class I MHC in the TBJ neuroblastoma cell line (Salcedo et al 2004).…”

Section: Il-27 Modulates Antigen Presentationmentioning

confidence: 99%

“…The latest studies assign new capabilities to IL-27: stimulation of hematopoiesis, enhancement of antigen presentation by antigen-presenting cells (APCs), inhibition of angiogenesis, and inhibition of HIV replication. Although the IL-27 receptor was initially thought to be expressed only by hematopoietic cells, new cell populations, including stem cells, vascular endothelium, and keratinocytes, have been found to be sensitive to IL-27 (Feng et al 2008;Fitzgerald et al 2007;Kanda and Watanabe 2008;Shimizu et al 2006).…”

Section: Introductionmentioning

confidence: 99%

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Interleukin-27: Biological Properties and Clinical Application

Jankowski

Kopiński

Goc

2010

Arch. Immunol. Ther. Exp.

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Interleukin (IL)-27 is a novel cytokine secreted by stimulated antigen-presenting cells. Initial studies on the biology of IL-27 provided evidence for its role in the initiation of T(H)1 responses; however, subsequent work has indicated that IL-27 has broad inhibitory effects on T(H)1, T(H)2, and T(H)17 subsets of T cells as well as the expansion of inducible regulatory T cells. The involvement of IL-27 in the regulation of angiogenesis and antiviral response has also recently been reported. The aim of this review is to highlight the potential areas of IL-27 clinical application, especially the management of neoplastic and viral diseases as well as autoimmune disorders, including rheumatoid arthritis and multiple sclerosis. The review will also serve to elaborate on the molecular mechanisms involved in the expression of this cytokine and signaling from the IL-27 receptor.

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Section: Il-27 Modulates Antigen Presentationmentioning

confidence: 99%

Section: Il-27 Modulates Antigen Presentationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Interleukin-27: Biological Properties and Clinical Application

Jankowski

Kopiński

Goc

2010

Arch. Immunol. Ther. Exp.

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“…IL-27 acts on a wide range of immune cells, including CD4 + and CD8 + T lymphocytes, NK cells, monocytes/macrophages, and activated DCs (23,(26)(27)(28)(29). The effect of IL-27 on monocytes/macrophages is complex, as it is able to induce or suppress the expression of surface activation molecules or cytokines by these cells (23,28,(30)(31)(32). The pleiotropic effects of IL-27 on monocytes/ macrophages may depend on the timing and context of surrounding inflammatory signals and the nature of the local immune environment.…”

mentioning

confidence: 99%

IL-27/IFN-γ Induce MyD88-Dependent Steroid-Resistant Airway Hyperresponsiveness by Inhibiting Glucocorticoid Signaling in Macrophages

Wang

Baines

et al. 2010

The Journal of Immunology

131

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Inflammation and airway hyperresponsiveness (AHR) are hallmark features of asthma and often correlate with the severity of clinical disease. Although these features of asthma can be effectively managed with glucocorticoid therapy, a subgroup of patients, typically with severe asthma, remains refractory to therapy. The mechanisms leading to steroid resistance in severe asthmatics are poorly understood but may be related to the activation of innate host defense pathways. Previously, we have shown that IFN-γ–producing cells and LPS, two factors that are associated with severe asthma, induce steroid-resistant AHR in a mouse model. We now demonstrate that cooperative signaling induced by IFN-γ and LPS results in the production of IL-27 by mouse pulmonary macrophages. IL-27 and IFN-γ uniquely cooperate to induce glucocorticoid-resistant AHR through a previously unknown MyD88-dependent mechanism in pulmonary macrophages. Importantly, integrated signaling by IL-27/IFN-γ inhibits glucocorticoid-induced translocation of the glucocorticoid receptor to the nucleus of macrophages. Furthermore, expression of both IL-27 and IFN-γ was increased in the induced sputum of steroid-refractory asthmatics. These results suggest that a potential mechanism for steroid resistance in asthma is the activation of MyD88-dependent pathways in macrophages that are triggered by IL-27 and IFN-γ, and that manipulation of these pathways may be a therapeutic target.

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“…Besides the effect of IL-27 on the Th17 cell lineage other anti-inflammatory properties of IL-27 have been demonstrated. These mostly comprise the production of the anti-inflammatory cytokine IL-10 through mechanisms involving STAT3, 123 cMAF, and ICOS, 124 although other pathways including the suppression of cFos, 115 B-cell class switching, 125 and enhanced TLR responsiveness 126 have also been described.…”

Section: à7mentioning

confidence: 99%

Genetics of childhood-onset inflammatory bowel disease

Henderson

Limbergen

Wilson

et al. 2011

Inflammatory Bowel Diseases

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Nearly a third of inflammatory bowel disease (IBD) patients present in childhood or adolescence, with epidemiological and natural history studies clearly demonstrating a rising incidence in this population. Although early-onset disease has a distinct phenotype, such as more extensive disease at onset and rapid progression, two recent genome-wide association studies (GWAS) carried out exclusively in this age group have demonstrated marked genetic similarities to adult disease. Although these parallels exist, this review will focus on the novel regions associated with early-onset IBD susceptibility identified by these early-onset GWAS. These new loci reaffirm the dysregulated pathways previously implicated in adult IBD pathogenesis and provide further insight into the pathophysiology of intestinal inflammation. The newly identified loci and expression data suggest mutations in genes encoding IL-27, which is involved in Th17 effector cell physiology; MTMR3, which we demonstrate is an essential component of autophagy; and CAPN10, which is necessary in regulating endoplasmic reticulum stress. In addition, the roles of PSMG1, TNFRSF6B, ZMIZ1 and SMAD3 are also discussed in relation to abnormal protein degradation and the secondary immune response. It is clear that with increasing technology our understanding of IBD pathogenesis is deepening at the genomic level and that the use of early patient selection coupled with ongoing work on therapeutic targets will lead to improved disease-modifying treatments in the near future.

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Regulation of the class II and class I MHC pathways in human THP-1 monocytic cells by interleukin-27

Cited by 37 publications

References 18 publications

Interleukin-27: Biological Properties and Clinical Application

Interleukin-27: Biological Properties and Clinical Application

IL-27/IFN-γ Induce MyD88-Dependent Steroid-Resistant Airway Hyperresponsiveness by Inhibiting Glucocorticoid Signaling in Macrophages

Genetics of childhood-onset inflammatory bowel disease

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