ORIGINAL ARTICLE: Tumor Necrosis Factor (TNF)-TNF Receptor Gene Polymorphisms and Their Serum Levels in Korean Women with Endometriosis

Abstract Background Idiopathic intracranial hypertension (IIH) is a neurological disorder of unknown pathophysiology with many proposed theories that involve CSF dynamics but recently, involvement of inflammatory and autoimmune processes has been postulated. Objectives To investigate presence of oligoclonal bands (OCB) in cerebrospinal fluid (CSF) and serum cytokine level in patients with IIH. Methods This study was conducted on 27 IIH female patients and 21 age- and sex-matched control groups. Patient and control groups were subjected to measurement of interleukin-4 (IL-4), IL-10, and tumor necrosis factor α (TNF-α) levels in serum, and CSF oligoclonal bands was measured in the IIH patient group. Body mass index (BMI) was measured to both patients and control. Results Serum levels of IL-4, IL-10, and TNF alpha were significantly higher in IIH patients than controls (p < 0.001); 22% of IIH patients had positive OCB in CSF. There was a statistically significant difference regarding TNF-α level in OCB-positive and OCB-negative patients being higher in positive patients. No statistically significant correlation was found between serum levels of IL-4, IL-10, TNF-α, and BMI. Conclusion Autoimmune inflammatory process may play a role in pathophysiology of IIH.

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The α and β Subunits of IκB Kinase (IKK) Mediate TRAF2-Dependent IKK Recruitment to Tumor Necrosis Factor (TNF) Receptor 1 in Response to TNF

Molecular and Cellular Biology ◽

10.1128/mcb.21.12.3986-3994.2001 ◽

2001 ◽

Vol 21 (12) ◽

pp. 3986-3994 ◽

Cited By ~ 100

Author(s):

Anne Devin ◽

Yong Lin ◽

Shoji Yamaoka ◽

Zhiwei Li ◽

Michael Karin ◽

...

Keyword(s):

Tumor Necrosis Factor ◽

Tumor Necrosis ◽

Leucine Zipper ◽

Nuclear Translocation ◽

Ring Finger ◽

Tnf Receptor ◽

Death Domain ◽

Iκb Kinase ◽

Cytokine Tumor Necrosis Factor ◽

Necrosis Factor

ABSTRACT The activation of IκB kinase (IKK) is a key step in the nuclear translocation of the transcription factor NF-κB. IKK is a complex composed of three subunits: IKKα, IKKβ, and IKKγ (also called NEMO). In response to the proinflammatory cytokine tumor necrosis factor (TNF), IKK is activated after being recruited to the TNF receptor 1 (TNF-R1) complex via TNF receptor-associated factor 2 (TRAF2). We found that the IKKα and IKKβ catalytic subunits are required for IKK-TRAF2 interaction. This interaction occurs through the leucine zipper motif common to IKKα, IKKβ, and the RING finger domain of TRAF2, and either IKKα or IKKβ alone is sufficient for the recruitment of IKK to TNF-R1. Importantly, IKKγ is not essential for TNF-induced IKK recruitment to TNF-R1, as this occurs efficiently in IKKγ-deficient cells. Using TRAF2−/− cells, we demonstrated that the TNF-induced interaction between IKKγ and the death domain kinase RIP is TRAF2 dependent and that one possible function of this interaction is to stabilize the IKK complex when it interacts with TRAF2.

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