TRAF6 is a critical signal transducer in IL-33 signaling pathway

Funakoshi‐Tago, Megumi; Tago, Kenji; Hayakawa, Morisada; Tominaga, Shin Ichi; Ohshio, Tomoyuki; Sonoda, Yoshiko; Kimura, Tadashi

doi:10.1016/j.cellsig.2008.05.013

Cited by 127 publications

(108 citation statements)

References 37 publications

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“…The provocative cytokines result in the over-expression of inflammation-mediated genes and accordingly release toxic molecules, which increase demyelination (42)(43)(44). Activation of NF-κB and Toll-like receptor signaling pathways stimulates TNF-α or IL-1β, which mediates IL-33 transcription (21,27,45,46).…”

Section: Discussionmentioning

confidence: 99%

“…One of the most important cytokines that directly contributes to the immunopathogenesis of MS is IL-33 (17), a recently discovered cytokine, taking part in various inflammatory and autoimmune diseases like psoriasis, lupus erythematous, ulcerative colitis and MS (17)(18)(19)(20). ST2L, a receptor of IL-33, is expressed on the surface of various subsets of leukocytes and conducts signals to activate the MAPK and nuclear factor κB (NF-κB) pathways by TNF receptor-associated factor 6 (TRAF6) (21,22). The IL-33/ST2 pathway is pivotal to inflammatory responses and autoimmune disorders (23).…”

Section: Introductionmentioning

confidence: 99%

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Interleukin-33 plasma levels in patients with relapsing-remitting multiple sclerosis

Alsahebfosoul

Rahimmanesh

Shajarian

et al. 2017

Biomolecular Concepts

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Cytokines are implicated in the immunopathogenesis of multiple sclerosis (MS). Interleukin (IL)-33, one of the recently discovered members of the IL-1 superfamily, is a dual functional cytokine involved in various autoimmune disorders. In a case-control study, venous blood was collected from healthy subjects categorized as control group (n = 44) and MS patients (n = 44). All recruited patients were clinically diagnosed with relapsing-remitting MS (RRMS), including patients without treatment (new identified cases, n = 16) and those treated with interferon beta (IFN-β) (n = 28). The plasma levels of IL-33 in subjects were measured with ELISA. Significantly elevated IL-33 plasma levels were observed in RRMS patients (p = 0.005). Furthermore, IFN-β-treated MS patients had lower levels of IL-33 compared to the untreated patients (p < 0.001). Increased IL-33 plasma levels in the patient group might be associated with development of MS. These results could contribute to our better understanding about the role of IL-33 in the immunopathogenesis of MS.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Interleukin-33 plasma levels in patients with relapsing-remitting multiple sclerosis

Alsahebfosoul

Rahimmanesh

Shajarian

et al. 2017

Biomolecular Concepts

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“…Bunlardan ST2L; transmembran formdur ve IL-33 ile birleflerek IL-1R aksesuar proteine ba¤lan›p kompleks oluflturur. [8] Bu kompleks daha sonra nükleer faktör κβ (NF-κβ) ve mitojenle aktive olmufl protein (MAP) kinazlar arac›l›¤› ile Th2 tip sitokin sal›n›m›na yol açarak IL-33'ün proinflamatuar etkisi ortaya ç›kar. [5,7,8] IL-33 ayr›ca Th2 hücreleri için kemoattraktan görevi de görür.…”

Section: Il-33 Ve St2unclassified

The role of IL-33 in Behçet's disease

Dinçer¹,

Yayla²,

Ateş³

2017

RAED Derg

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“…MyD88 (myeloid differentiation factor 88), IRAK-4 (interleukin-1 receptor-associated kinase 4), IRAK-1, and TRAF6 (TNF-␣ receptor-associated factor 6) are also recruited to ST2L, similar to other members of the IL-1R/TLR superfamily (3,7). The activation of these pathways results in the phosphorylation of the MAPKs ERK1/2, p38, and JNK.…”

mentioning

confidence: 99%

“…In addition, the phosphorylation and degradation of IB␣ (inhibitor of B␣) allows the NF-B protein subunits p50 and p65 to enter the nucleus and induce gene expression (8). Both MyD88 and TRAF6 are required for the activation of NF-B, p38, and JNK, whereas ERK activation can occur in the absence of TRAF6 (7). IL-33 is an endogenous proinflammatory danger signal that is released from damaged or dying cells (9,10), and the IL-33/ST2L signaling axis has been implicated in numerous conditions, notably certain allergic and cardiovascular diseases (11,12).…”

mentioning

confidence: 99%

The GOLD Domain-containing Protein TMED1 Is Involved in Interleukin-33 Signaling*

Connolly

O’Neill

McGettrick

2013

Journal of Biological Chemistry

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Background: A putative association between the trafficking protein TMED1 and the IL-33 receptor ST2L has previously been reported; however, the functional consequence of this remained unknown. Results: TMED1 binds ST2L, and TMED1 knockdown impairs IL-33-induced IL-8 and IL-6 production. Conclusion: TMED1 is required for optimal IL-33-induced signal activation. Significance: These results further implicate the TMED family as an important family in immune signaling pathways.

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TRAF6 is a critical signal transducer in IL-33 signaling pathway

Cited by 127 publications

References 37 publications

Interleukin-33 plasma levels in patients with relapsing-remitting multiple sclerosis

Interleukin-33 plasma levels in patients with relapsing-remitting multiple sclerosis

The role of IL-33 in Behçet's disease

The GOLD Domain-containing Protein TMED1 Is Involved in Interleukin-33 Signaling*

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