IL-31 is associated with cutaneous lymphocyte antigen–positive skin homing T cells in patients with atopic dermatitis

Bilsborough, Janine; Leung, Donald Y.M.; Maurer, Mark; Howell, Michael D.; Boguniewcz, Mark; Yao, Lena; Storey, H. H.; LeCiel, Cosette; Harder, Brandon; Gross, Jane A.

doi:10.1016/j.jaci.2005.10.046

Cited by 321 publications

(287 citation statements)

References 28 publications

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“…In a nontransgenic murine model of spontaneous AD development, increased levels of IL-31 mRNA were associated with scratching behavior (24,25), and subsequent inhibition of scratching was achieved using a neutralizing anti-IL-31 mAb (15). Finally, increased levels of IL-31 mRNA have been associated with samples from human AD patients (2,5), and these IL-31 levels were further shown to correlate with increases in IL-4 and IL-13 (3).…”

Section: Discussionmentioning

confidence: 96%

“…Overexpression of IL-31 in transgenic mice results in a pruritic skin condition that is similar to human atopic dermatitis (AD) (1). Moreover, analysis of IL-31 levels in human dermatitis samples has shown increased expression of IL-31 in AD, prurigo nodularis, and allergic contact dermatitis compared with healthy control populations (2)(3)(4)(5). IL-31 expression has also been shown to correlate with the expression of the Th2 cytokines IL-4 and IL-13 in human skin disease samples, implicating IL-31 in the pathogenesis of allergic skin diseases (3).…”

Section: Nterleukin-31 Is Produced By Activated Cd4mentioning

confidence: 99%

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IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M

Bilsborough

Mudri²,

Chadwick³

et al. 2010

The Journal of Immunology

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IL-31 signals through the heterodimeric receptor IL-31RA and oncostatin M receptor (OSMR), and has been linked with the development of atopic dermatitis, a Th2 cytokine-associated disease in humans. However, recent studies of IL-31RA knockout (KO) mice have suggested that IL-31 signaling may be required to negatively regulate Th2 type responses rather than exacerbate them. Because those studies were performed on genetically modified mice, we examined whether neutralizing IL-31 with a specific mAb would give similar results to IL-31RA KO mice in two Th2 cytokine-associated immune models. We report no difference in lymphocyte Th2-type cytokine production after Ag immunization between IL-31RA KO mice, mice treated with the IL-31 mAb, or control animals. Second, we tested whether the absence of the IL-31RA subunit in IL-31RA KO mice may allow for increased pairing of the OSMR subunit with another cytokine receptor, gp130, resulting in overrepresentation of the heterodimeric receptor for OSM and increased responsiveness to OSM protein. We found that intranasal OSM challenge of IL-31RA KO mice resulted in increased IL-6 and vascular endothelial growth factor production in the lung compared with wild-type littermate control animals. Moreover, PBS-challenged IL-31RA KO mice already had increased levels of vascular endothelial growth factor, which were further increased by OSM challenge. These data imply that IL-31RA–deficient mice produce increased levels of OSM-inducible cytokines during airway sensitization and challenge, which may be the driving force behind the apparent exacerbation of Th2-type inflammatory responses previously observed in these mice.

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Section: Discussionmentioning

confidence: 96%

Section: Nterleukin-31 Is Produced By Activated Cd4mentioning

confidence: 99%

IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M

Bilsborough

Mudri²,

Chadwick³

et al. 2010

The Journal of Immunology

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“…The transcripts and protein levels of IL-31 and the number of Th2 cells that secrete IL-31 are elevated in various skin diseases including atopic dermatitis, atopic contact dermatitis, and purigo nodularis (7)(8)(9). IL-31 is thought to play an important role in the induction of pruritus, which is a characteristic feature of these skin diseases (10).…”

Section: Interleukin 31 Receptor ␣ (Il-mentioning

confidence: 99%

Th2 Cytokines Augment IL-31/IL-31RA Interactions via STAT6-dependent IL-31RA Expression

Edukulla

Singh

Jegga

et al. 2015

Journal of Biological Chemistry

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Background: IL-31RA is a novel Type I cytokine receptor that pairs with oncostatin M receptor to mediate IL-31 signaling. Results: Th2 cytokines up-regulate IL-31RA signaling in macrophages. Conclusion: We demonstrate that the Th2 cytokines IL-4 and IL-13 were capable of up-regulating IL-31RA expression on macrophages. Significance: This newly identified counter-regulatory role between Th2 cytokine and the IL-31 signaling cascade may provide valuable insights into the pathobiology of allergic diseases.

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“…As in the case of IL-13, transgenic overexpression of IL-31 also induced severe pruritus and dermatitis in mice [144]. 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].…”

Section: Inflammatory Mediators As Peripheral Itch Sensitizersmentioning

confidence: 52%

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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IL-31 is associated with cutaneous lymphocyte antigen–positive skin homing T cells in patients with atopic dermatitis

Cited by 321 publications

References 28 publications

IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M

IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M

Th2 Cytokines Augment IL-31/IL-31RA Interactions via STAT6-dependent IL-31RA Expression

TRP Channels and Pruritus

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