Signaling by IL-31 and functional consequences

Cornélissen, Christian; Lüscher-Firzlaff, Juliane; Baron, Jens Malte; Lüscher, Bernhard

doi:10.1016/j.ejcb.2011.07.006

Cited by 180 publications

(201 citation statements)

References 107 publications

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“…39 Although we could find no effect of IL-31 on osteoblast or osteoclast differentiation in vitro, 25 IL-31RA deletion has been noted to increase hepatic cytokine response to OSM. 40 This suggests that OSMR deletion may increase responses to other gp130-dependent cytokines by increasing the availability of other receptor components.…”

Section: The Influence Of Osmr In the Action Of Pthmentioning

confidence: 44%

Osteoimmunology: oncostatin M as a pleiotropic regulator of bone formation and resorption in health and disease

Sims

Quinn

2014

BoneKEy Reports

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Bone remodeling in health and disease is carried out by osteoblasts and osteoclasts, which respectively produce bone matrix and resorb it. Endocrine and paracrine control of these cells can be direct, but they are also exerted indirectly, either by influencing progenitor cell differentiation or by stimulating paracrine signals from local accessory cells including osteocytes (which form a critical communication and regulation network within the bone matrix), macrophages and T lymphocytes. Here we review the osteotropic actions of the interleukin-6 family member cytokine oncostatin M (OSM), which is of particular interest because of its ability to stimulate bone accrual. OSM is produced within the bone microenvironment by cells of both mesenchymal and hematopoietic origin, including osteocytes, osteoblasts, macrophages and T lymphocytes, and can act via two receptor complexes: OSM receptor:gp130 and leukemia inhibitory factor receptor (LIFR):gp130. Although OSM can directly stimulate osteoblast mineralization activity and differentiation, it can also stimulate mesenchymal stem cell osteoblastic commitment at the expense of adipogenesis. In osteocytes, OSM can suppress the production of the bone formation inhibitor sclerostin, an action that is mediated by LIFR:gp130. OSM also stimulates the production of receptor activator of nuclear factor kB ligand by osteoblasts and thereby drives the formation of osteoclasts particularly in pathological conditions. Thus, cellular effects of OSM on bone metabolism include direct and indirect actions mediated by two related receptor/ligand complexes. OSM therefore provides an example of paracrine and endocrine control mechanisms that regulate bone mass by controlling both bone formation and resorption.

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Section: The Influence Of Osmr In the Action Of Pthmentioning

confidence: 44%

Osteoimmunology: oncostatin M as a pleiotropic regulator of bone formation and resorption in health and disease

Sims

Quinn

2014

BoneKEy Reports

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“…However, the marked increase of the Th2 cytokine IL-31 and pronounced rapid antibody production demonstrate an active antiparasitic process. IL-31 has been associated with inflammatory processes in Th2-dependent pathologies, such as asthma (22). This suggests that the resistance against reinfection of Swiss-Webster mice is indeed mediated by an active local immune response, possibly mediated by antibody or other specific Th2-type mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-6-Driven Inflammatory Response Induces Retinal Pathology in a Model of Ocular Toxoplasmosis Reactivation

et al. 2015

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c Ocular inflammation is one of the consequences of infection with the protozoan parasite Toxoplasma gondii. Even if lesions are self-healing in immunocompetent persons, they pose a lifetime risk of reactivation and are a serious threat to vision. As there are virtually no immunological data on reactivating ocular toxoplasmosis, we established a model of direct intravitreal injection of parasites in previously infected mice with a homologous type II strain. Two different mouse strains with variable ability to control retinal infection were studied in order to describe protective and deleterious reaction patterns. In Swiss-Webster mice, which are already relatively resistant to primary infection, no peak of parasite load was observed upon reinfection. In contrast, the susceptible inbred strain C57BL/6 showed high parasite loads after 7 days, as well as marked deterioration of retinal architecture. Both parameters were back to normal on day 21. C57BL/6 mice also reacted with a strong local production of inflammatory and Th1-type cytokines, like interleukin-6 (IL-6), IL-17A, and gamma interferon (IFN-␥), while Swiss-Webster mice showed only moderate expression of the Th2 cytokine IL-31. Interestingly, rapid intraocular production of anti-Toxoplasma antibodies was observed in Swiss-Webster but not in C57BL/6 mice. We then localized the cellular source of different immune mediators within the retina by immunofluorescence. Finally, neutralization experiments of IFN-␥ or IL-6 demonstrated the respective protective and deleterious roles of these cytokines for parasite control and retinal integrity during reinfection. In conclusion, we developed and immunologically characterized a promising mouse model of reactivating ocular toxoplasmosis. O cular toxoplasmosis (OT), a sequel of infection with the apicomplexan parasite Toxoplasma gondii, is a major cause of visual impairment worldwide, responsible for 30 to 50% of posterior uveitis in immunocompetent people. While OT was considered until recently as being exclusively due to congenital infection, screening of Toxoplasma-seropositive persons in Europe and North America revealed that 1 to 2% of this population presents retinal toxoplasmic lesions (1). Thus, possible reactivation of these ocular infections in postnatally infected individuals poses a hitherto underestimated problem for the health systems in these countries (2) and even more so in regions like South America (3, 4). At the moment, no treatment has so far achieved a consistently reduced risk of reactivation, except perhaps in high-risk patients (5, 6). To establish more specific, immune-based interventions, we need to elucidate the physiopathology of OT, which is so far largely ignored. Therefore, we wanted to gather novel data on the immune responses involved in retinal T. gondii reactivation. The long-term objective of this model is to open new therapeutic perspectives of human OT.The main obstacle for thorough research of ocular reactivation is the absence of a suitable mouse model (4). After oral or intraper...

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“…IL-31RAv1 is homologous to human IL-31RAv4 and is expressed as a membranebound form, whereas IL-31RAv2 is a soluble form consisting of a cytokine-binding domain and fibronectin type III domains (1,2). Both the membrane-bound and soluble forms of the receptor bind to IL-31 with comparable affinity and initiate intracellular signal transduction resulting in secretion of several proinflammatory cytokines and chemokines, which play a critical role in Th2 cytokine-mediated inflammatory diseases (3,4). Although the expression and distribution of IL-31RA in different cells or tissues have not been well studied, IL-31RA is constitutively expressed by non-hematopoietic cells, such as lung epithelial cells, and also exhibits limited expression on activated monocytes and eosinophils (1,5,6).…”

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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Signaling by IL-31 and functional consequences

Cited by 180 publications

References 107 publications

Osteoimmunology: oncostatin M as a pleiotropic regulator of bone formation and resorption in health and disease

Osteoimmunology: oncostatin M as a pleiotropic regulator of bone formation and resorption in health and disease

Interleukin-6-Driven Inflammatory Response Induces Retinal Pathology in a Model of Ocular Toxoplasmosis Reactivation

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

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