000065288 001__ 65288
000065288 005__ 20201105083209.0
000065288 0247_ $$2doi$$a10.3389/fimmu.2017.01739
000065288 0248_ $$2sideral$$a104273
000065288 037__ $$aART-2017-104273
000065288 041__ $$aeng
000065288 100__ $$aFrejo, L.
000065288 245__ $$aRegulation of Fn14 receptor and NF-¿B underlies inflammation in Meniere's disease
000065288 260__ $$c2017
000065288 5060_ $$aAccess copy available to the general public$$fUnrestricted
000065288 5203_ $$aMeniere''s disease (MD) is a rare disorder characterized by episodic vertigo, sensorineural hearing loss, tinnitus, and aural fullness. It is associated with a fluid imbalance between the secretion of endolymph in the cochlear duct and its reabsorption into the subarachnoid space, leading to an accumulation of endolymph in the inner ear. Epidemiological evidence, including familial aggregation, indicates a genetic contribution and a consistent association with autoimmune diseases (AD). We conducted a case-control study in two phases using an immune genotyping array in a total of 420 patients with bilateral MD and 1, 630 controls. We have identified the first locus, at 6p21.33, suggesting an association with bilateral MD [meta-analysis leading signal rs4947296, OR = 2.089 (1.661-2.627); p = 1.39 × 10-09]. Gene expression profiles of homozygous genotype-selected peripheral blood mononuclear cells (PBMCs) demonstrated that this region is a trans-expression quantitative trait locus (eQTL) in PBMCs. Signaling analysis predicted several tumor necrosis factor-related pathways, the TWEAK/Fn14 pathway being the top candidate (p = 2.42 × 10-11). This pathway is involved in the modulation of inflammation in several human AD, including multiple sclerosis, systemic lupus erythematosus, or rheumatoid arthritis. In vitro studies with genotype-selected lymphoblastoid cells from patients with MD suggest that this trans-eQTL may regulate cellular proliferation in lymphoid cells through the TWEAK/Fn14 pathway by increasing the translation of NF-¿B. Taken together; these findings suggest that the carriers of the risk genotype may develop an NF-¿B-mediated inflammatory response in MD.
000065288 536__ $$9info:eu-repo/grantAgreement/ES/FEDER/ISCIII/PI13-1242
000065288 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000065288 590__ $$a5.511$$b2017
000065288 591__ $$aIMMUNOLOGY$$b30 / 155 = 0.194$$c2017$$dQ1$$eT1
000065288 592__ $$a2.803$$b2017
000065288 593__ $$aImmunology and Allergy$$c2017$$dQ1
000065288 593__ $$aImmunology$$c2017$$dQ1
000065288 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000065288 700__ $$aRequena, T.
000065288 700__ $$aOkawa, S.
000065288 700__ $$aGallego-Martinez, A.
000065288 700__ $$aMartinez-Bueno, M.
000065288 700__ $$aAran, I.
000065288 700__ $$aBatuecas-Caletrio, A.
000065288 700__ $$aBenitez-Rosario, J.
000065288 700__ $$aEspinosa-Sanchez, J.M.
000065288 700__ $$0(orcid)0000-0002-6561-3305$$aFraile-Rodrigo, J.J.
000065288 700__ $$aGarcía-Arumi, A.M.
000065288 700__ $$aGonzález-Aguado, R.
000065288 700__ $$aMarques, P.
000065288 700__ $$aMartin-Sanz, E.
000065288 700__ $$aPerez-Fernandez, N.
000065288 700__ $$aPérez-Vázquez, P.
000065288 700__ $$aPerez-Garrigues, H.
000065288 700__ $$aSantos-Perez, S.
000065288 700__ $$aSoto-Varela, A.
000065288 700__ $$aTapia, M.C.
000065288 700__ $$aTrinidad-Ruiz, G.
000065288 700__ $$aSol, A.
000065288 700__ $$aAlarcon Riquelme, M.E.
000065288 700__ $$aLopez-Escamez, J.A.
000065288 773__ $$g8 (2017), 1739 [15 pp]$$pFront. immunol.$$tFRONTIERS IN IMMUNOLOGY$$x1664-3224
000065288 8564_ $$s480065$$uhttps://zaguan.unizar.es/record/65288/files/texto_completo.pdf$$yVersión publicada
000065288 8564_ $$s109515$$uhttps://zaguan.unizar.es/record/65288/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
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000065288 951__ $$a2020-11-05-08:20:18
000065288 980__ $$aARTICLE