Complete overlap of interleukin-31 receptor A and oncostatin M receptor β in the adult dorsal root ganglia with distinct developmental expression patterns

Bando, T.; Morikawa, Yoshihiro; Komori, Tadasuke; Senba, Emiko

doi:10.1016/j.neuroscience.2006.07.009

Cited by 100 publications

(75 citation statements)

References 24 publications

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“…IL-31 transgenic mice spontaneously develop the symptoms of AD (2). Furthermore, enhanced levels of IL-31RA and OSMR-b are closely related with itching behavior in AD mice (15), and treatment with anti-IL-31 Ab inhibits the scratching behavior of the NC/Nga mouse (16).…”

mentioning

confidence: 99%

NFAT1 and JunB Cooperatively Regulate IL-31 Gene Expression in CD4+ T Cells in Health and Disease

Hwang

Kim

Park

et al. 2015

The Journal of Immunology

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IL-31 is a key mediator of itching in atopic dermatitis (AD) and is preferentially produced by activated CD4+ T cells and Th2 cells. Although pathophysiological functions of IL-31 have been suggested in diverse immune disorders, the molecular events underlying IL-31 gene regulation are still unclear. In this study we identified the transcription start site and functional promoter involved in IL-31 gene regulation in mouse CD4+ T cells. TCR stimulation–dependent IL-31 expression was found to be closely linked with in vivo binding of NFAT1 and JunB to the IL-31 promoter. Although NFAT1 alone enhanced IL-31 promoter activity, it was further enhanced in the presence of JunB. Conversely, knockdown of either NFAT1 or JunB resulted in reduced IL-31 expression. NFAT1-deficient CD4+ T cells showed a significant defect in IL-31 expression compared with wild-type CD4+ T cells. In agreement with these findings, mice subjected to atopic conditions showed much higher levels of IL-31, which were closely correlated with a significant increase in the number of infiltrated NFAT1+CD4+ T cells into the AD ears. Amelioration of AD progression by cyclosporin A treatment was well correlated with downregulation of IL-31 expressions in CD4+ T cells and total ear residual cells. In summary, our results suggest a functional cooperation between NFAT1 and JunB in mediating IL-31 gene expression in CD4+ T cells and indicate that interference with this interaction or their activity has the potential of reducing IL-31–mediated AD symptoms.

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mentioning

confidence: 99%

NFAT1 and JunB Cooperatively Regulate IL-31 Gene Expression in CD4+ T Cells in Health and Disease

Hwang

Kim

Park

et al. 2015

The Journal of Immunology

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“…14) as a member of the IL-6R group that does not engage gp130, but OSMR␤, to form a signaling receptor complex (15,16). Based on the effects of ectopic expression in transgenic mice, IL-31, a CD4 ϩ T-cell-derived cytokine, has been associated with pruritis and dermatitis affecting dermal keratinocytes and dorsal root ganglia (17)(18)(19). Because antigenic challenge increased levels of IL-31 in a mouse model of airway hyper-responsiveness, this cytokine has also been proposed to play a role in airway hypersensitivity (15).…”

mentioning

confidence: 99%

“…Considering the limitations of transient expression systems, the precise function of the IL-31R complex beyond the immediate signaling reactions and quantitative comparison to the action by the other IL-6 cytokine receptors remains to be determined. Despite the prediction of IL-31-responsive epidermal keratinocytes and other epithelial cells (15,(17)(18)(19), the study of the receptor signaling in these cells proved to be challenging because the level of IL-31R␣ is low relative to that of OSMR␤.…”

mentioning

confidence: 99%

Interleukin-31 and Oncostatin-M Mediate Distinct Signaling Reactions and Response Patterns in Lung Epithelial Cells

Chattopadhyay

Tracy

Liang

et al. 2007

Journal of Biological Chemistry

121

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Many mammalian cell types co-express several receptors for the evolutionarily related hematopoietic cytokines of the interleukin (IL) 4 -6 group (1). Moreover, all cell types express gp130, the common signal-transducing subunit of this receptor family. A major unresolved issue is whether the receptors for the individual IL-6 cytokines exert redundant functions because of the involvement of shared subunits, or whether they exert specific actions because of the formation of heteromeric subunit combinations. Gross analyses of cell responses to IL-6 cytokines indicated similar signaling reactions, supporting the notion of redundancy (2, 3). However, the individual receptor forms determine not only the ability of the cells to respond to specific IL-6 cytokines by mediating ligand binding but also the quantitative signaling by the relative expression levels of receptor subunits (4). The model of IL-6 cytokine receptors directing specific action takes into consideration that receptor complexes engage cytoplasmic domains of two signal-transducing subunits with distinct structures and capabilities to communicate to signaling pathways (3, 5). The ligand-dependent association of receptor subunits into signaling-competent complexes leads invariably to the activation of JAKs and to a specific pattern of auto-and trans-tyrosine phosphorylation of kinases, receptor subunits, and interacting proteins, including STATs, Src homology 2-containing phosphatase 2, Src homology 2-containing protein C (SHC) and other adaptor proteins. The receptor proximal events at the plasma membrane and the level of sustained signaling defines the duration and magnitude of cell responses, including transcriptional induction of genes, altered cell morphology, and changes in cell proliferation. Proliferation control by cytokine-activated STAT proteins has gained particular attention in part to explain the role of IL-6 cytokines in tissue damage repair (6 -8) and potential relevance to support tumorigenesis (9, 10). Unexplained thus far is the basis for the divergent outcome of IL-6 cytokine action that, in certain epithelial cell types, yields a suppression of proliferation (11), whereas in other cell types it yields a growth promotion (12, 13). Because the subunits for IL-6 cytokine receptors are encoded by single-copy genes, comparable structures and biochemical actions are expected for the receptor proteins expressed in the various cell types, regardless of the ultimate outcome of cytokine treatment.An independent assessment of receptor signaling specificity among IL-6 cytokine receptors became possible with the identification of IL-31R␣ (gp130-like protein; see Ref. 14) as a member of the IL-6R group that does not engage gp130, but OSMR␤, to form a signaling receptor complex (15,16). Based on the effects of ectopic expression in transgenic mice, IL-31, a CD4 ϩ T-cell-derived cytokine, has been associated with pruritis and dermatitis affecting dermal keratinocytes and dorsal root ganglia (17-19). Because antigenic challenge increased levels of * Th...

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“…Further supporting its role, increased expression of IL-31 was found both in an atopic mouse model [145] and in AD patients [146,147] in good correlation with the scratching behavior in mice [148] and the symptom severity in humans [149,150]. The exact pruritogenic mechanism of action of IL-31 is still unclear although IL-31 receptors were detected on a fraction of small diameter sensory neurons [151] as well as on normal human epidermal keratinocytes (NHEKs) [152]. On NHEKs, stimulation of toll-like receptor TLR-2 resulted in the elevation of IL-31 receptor expression levels, followed by an enhanced secretion of the pro-inflammatory chemokine ligand CCL2 (also known as monocyte chemotractic protein-1).…”

Section: Inflammatory Mediators As Peripheral Itch Sensitizersmentioning

confidence: 96%

TRP Channels and Pruritus

Tóth¹,

Bı́ró²

2013

TOPAINJ

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Itch (pruritus) is one of the most often seen sensory phenomena in clinical practice. Recent neurophysiological findings proposed the existence of a novel pruriceptive system which includes a multitude of pruritogenic (itch-inducing) peripheral mediators, itch-selective pruriceptors, sensory afferent networks, spinal cord neurons, and certain central nervous system regions. In this review, we first introduce major features of the pruriceptive system. We then focus on defining the roles of transient receptor potential (TRP) ion channels in skin-coupled itch and provide compelling evidence that certain thermosensitive TRP channels (especially TRPV1, TRPV3, TRPV4, and TRPA1) are indeed key players in pruritus pathogenesis. Finally, we propose TRP-centered future experimental directions towards the therapeutic targeting of TRP channels in the clinical management of itch.

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Complete overlap of interleukin-31 receptor A and oncostatin M receptor β in the adult dorsal root ganglia with distinct developmental expression patterns

Cited by 100 publications

References 24 publications

NFAT1 and JunB Cooperatively Regulate IL-31 Gene Expression in CD4+ T Cells in Health and Disease

NFAT1 and JunB Cooperatively Regulate IL-31 Gene Expression in CD4+ T Cells in Health and Disease

Interleukin-31 and Oncostatin-M Mediate Distinct Signaling Reactions and Response Patterns in Lung Epithelial Cells

TRP Channels and Pruritus

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