Type II Collagen Autoimmunity in Otosclerosis and Meniere's Disease

Yoo, T. J.; Stuart, J.; Kang, Andrew H.; Townes, Alexander S.; Tomoda, Koichi; Dixit, Saryu N.

doi:10.1126/science.7112122

Cited by 207 publications

(69 citation statements)

References 9 publications

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“…On immunizing rats with collagen type II lesions resembling otosclerotic foci within the otic capsule were present in animals which were observed for more than 6 months after immunization [34]. Antibodies against collagen II were described by Yoo et al [35] in the serum of patients suffering from otosclerosis and Ménière's disease. Bujia et al [36] found serum antibodies against collagen IX significantly increased in comparison with controls, while the antibodies against collagen II were not significantly raised.…”

Section: Collagen (Auto)immunitymentioning

confidence: 95%

Etiopathogenesis of Otosclerosis

Niedermeyer

Arnold

2002

ORL

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Otosclerosis is a frequent cause of nonsyndromic hearing loss which affects exclusively the human temporal bone. Various etiopathogenetic hypotheses have been proposed. The major hypotheses considered are genetic factors, immunologic factors and viral infection. Since the familial incidence of otosclerosis is known a recent genetic analysis has given evidence of three otosclerosis genes (OTSC1–3). Mutations in the collagen gene COL1A1 have been found in one large family with several cases of otosclerosis. Concerning an immunologic etiopathogenetic process, the presence of serum antibodies against collagen II and IX in patients with otosclerosis confirms the hypothesis of a collagen autoimmune mechanism. Finally as a possible cause of this chronic inflammatory disease morphologic and biochemical investigations have revealed a measles virus association. In conclusion, various etiopathogenetic factors may contribute to the genesis of otosclerosis.

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Section: Collagen (Auto)immunitymentioning

confidence: 95%

Etiopathogenesis of Otosclerosis

Niedermeyer

Arnold

2002

ORL

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“…In the SV joint, on the contrary, the cartilage matrices with the lack of the CS-56 immunolabeling were vividly labeled with the type II collagen immunostaining. Previously, a hypothesis suggesting has been proposed that otosclerosis results from autoimmunoreactivity to type II collagen present in the fetal cartilaginous remnants of the human body labyrinth, based on the increased concentrations of circulating antibody against type II collagen in the patients and on the induction of otosclerosis-like lesions by immunization of rodents with cartilage collagen [31,32]. Independent researchers, however, have been unable to confirm these results.…”

Section: Discussionmentioning

confidence: 99%

“…Clinically, otosclerosis is progressive disorder of temporal bone of unknown cause and pathogenesis [8]. Genetic factors are clearly involved, but measles virus infection and autoimmunity to collagen type II also might play contributing roles [5,14,17,18,25,32]. The most common location of an otosclerotic focus is the otic capsule anterior to the stapes footplate [5].…”

Section: Introductionmentioning

confidence: 99%

“…The SV joint, on the contrary, where the stapes footplate articulates the vestibular window through the annular ligament is quite different from the other ossicular joints, although both the vestibular surface and the rim of the stapes footplate are also covered with hyaline cartilage. So far, some reports are available on immunohistochemical investigations of the cartilage matrices, such as collagen type II [32,33] and chondroitin sulfate [29] immunostainings. In addition, Ye et al [29] suggested that chondroitin sulfate may play an important role in the development of otosclerotic lesions.…”

Section: Introductionmentioning

confidence: 99%

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Histochemical Characterization of the Rat Ossicular Joint Cartilage with a Special Reference to Stapediovestibular Joint

Ohashi

Sawaguchi

Ide

et al. 2005

Acta Histochem. Cytochem

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The stapes footplate articulates the vestibular window (stapediovestibular joint; SV joint). The SV joint is known as crucial region of otosclerosis. To shed a light on pathogenesis of otosclerosis, we have examined the histochemical characteristics of the rat ossicular joint cartilage. Interestingly, glycoconjugate histochemistry revealed that the cartilage matrix components of the SV joint were significantly different from those of the other ossicular joints, i.e. incudomalleolar (IM) and incudostapedial (IS) joints. Alcian blue, pH 2.5 and high-iron diamine procedures vividly stained the cartilage matrices of the IM and IS joints, while those of the SV joint were faintly stained. Chondroitin sulfate immunohistochemistry revealed intense labeling of the cartilage of the IM and IS joints, while the immunolabeling of the SV joint was negligible. On the contrary, keratan sulfate immunolabeling was discernible on the cartilage matrices of the SV joint, but not on those of the IM and IS joints. Type II collagen immunolabeling revealed that the marginal region of the IM and IS joint cartilage matrices was devoid of the immunostaining, while the SV joint cartilage matrices were uniformly labeled with this antibody. In this study, we have succeeded in demonstrating the histochemical characteristics of the rat SV joint cartilage matrices of which is quite different from those of the other ossicular joints.

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“…Relapsing polychondritis [1,2] is a rare systemic autoimmune disorder of unknown origin characterized by episodic inflammation of cartilaginous tissues throughout the body where collagen type II (CII) is the major protein [3,4,5,6]. Elastic cartilage of the ears and nose, hyaline cartilage of peripheral joints, vertebral fibrocartilage, tracheobronchial cartilage, as well as proteoglycan-rich structures of the inner ear, eye, heart, or blood vessels may all be affected.…”

Section: Introductionmentioning

confidence: 99%

Adoptive Cellular Gene Therapy for the Treatment of Experimental Autoimmune Polychondritis Ear Disease

Zhou

Liao²,

Guo³

et al. 2017

ORL

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In the past, the clinical therapy for autoimmune diseases, such as autoimmune polychondritis ear disease, was mostly limited to nonspecific immunosuppressive agents, which could lead to variable responses. Currently, gene therapy aims at achieving higher specificity and less adverse effects. This concept utilizes the adoptive transfer of autologous T cells that have been retrovirally transduced ex vivo to express and deliver immunoregulatory gene products to sites of autoimmune inflammation. In the animal model of collagen-induced autoimmune polychondritis ear disease (CIAPED), the adoptive transfer of IL-12p40-expressing collagen type II (CII)-specific CD4+ T-cell hybridomas resulted in a significantly lower disease incidence and severity compared with untreated or vector-only-treated animals. In vivo cell detection using bioluminescent labels showed that transferred CII-reactive T-cell hybridomas accumulated in the inflamed earlobes of the mice with CIAPED. In vitro analysis demonstrated that IL-12p40-transduced T cells did not affect antigen-specific T-cell activation or systemic anti-CII Ab responses. However, IL-12p40-transduced T cells suppressed IFN-γ and augmented IL-4 production, indicating their potential to act therapeutically by interrupting Th1-mediated inflammatory responses via augmenting Th2 responses. These results indicate that the local delivery of IL-12p40 by T cells could inhibit CIAPED by suppressing autoimmune responses at the site of inflammation.

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Type II Collagen Autoimmunity in Otosclerosis and Meniere's Disease

Cited by 207 publications

References 9 publications

Etiopathogenesis of Otosclerosis

Etiopathogenesis of Otosclerosis

Histochemical Characterization of the Rat Ossicular Joint Cartilage with a Special Reference to Stapediovestibular Joint

Adoptive Cellular Gene Therapy for the Treatment of Experimental Autoimmune Polychondritis Ear Disease

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