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201. Mighty mites

Author

Yamaguchi, Yasuyuki, primary, Ujiie, Hideyuki, additional, and Shimizu, Hiroshi, additional

Published
2017
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203. Type XVII collagen coordinates proliferation in the interfollicular epidermis

Author

Watanabe, Mika, primary, Natsuga, Ken, additional, Nishie, Wataru, additional, Kobayashi, Yasuaki, additional, Donati, Giacomo, additional, Suzuki, Shotaro, additional, Fujimura, Yu, additional, Tsukiyama, Tadasuke, additional, Ujiie, Hideyuki, additional, Shinkuma, Satoru, additional, Nakamura, Hideki, additional, Murakami, Masamoto, additional, Ozaki, Michitaka, additional, Nagayama, Masaharu, additional, Watt, Fiona M, additional, and Shimizu, Hiroshi, additional

Published
2017
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205. Author response: Type XVII collagen coordinates proliferation in the interfollicular epidermis

Author

Watanabe, Mika, primary, Natsuga, Ken, additional, Nishie, Wataru, additional, Kobayashi, Yasuaki, additional, Donati, Giacomo, additional, Suzuki, Shotaro, additional, Fujimura, Yu, additional, Tsukiyama, Tadasuke, additional, Ujiie, Hideyuki, additional, Shinkuma, Satoru, additional, Nakamura, Hideki, additional, Murakami, Masamoto, additional, Ozaki, Michitaka, additional, Nagayama, Masaharu, additional, Watt, Fiona M, additional, and Shimizu, Hiroshi, additional

Published
2017
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210. Japanese guidelines for the management of pemphigoid (including epidermolysis bullosa acquisita).

Author

Ujiie, Hideyuki, Iwata, Hiroaki, Yamagami, Jun, Nakama, Takekuni, Aoyama, Yumi, Ikeda, Shigaku, Ishii, Norito, Iwatsuki, Keiji, Kurosawa, Michiko, Sawamura, Daisuke, Tanikawa, Akiko, Tsuruta, Daisuke, Nishie, Wataru, Fujimoto, Wataru, Amagai, Masayuki, and Shimizu, Hiroshi

Abstract

The pemphigoid group is a category of autoimmune subepidermal blistering diseases in which autoantibodies deposit linearly at the epidermal basement membrane zone (BMZ). The main subtypes of pemphigoid mediated by immunoglobulin G autoantibodies are bullous pemphigoid (BP), mucous membrane pemphigoid (MMP) and epidermolysis bullosa acquisita (EBA). To establish the first guidelines approved by the Japanese Dermatological Association for the management of pemphigoid diseases, the Committee for Guidelines for the Management of Pemphigoid Diseases (Including EBA) was founded as part of the Study Group for Rare Intractable Skin Diseases under the Ministry of Health, Labor and Welfare Research Project on Overcoming Intractable Diseases. These guidelines aim to provide current information for the management of BP, MMP and EBA in Japan. Based on evidence, the guidelines summarize the clinical and immunological manifestations, pathophysiologies, diagnostic criteria, disease severity determination criteria, treatment algorithms and treatment recommendations. Because of the rarity of these diseases, there are few clinical studies with a high degree of evidence, so several parts of these guidelines were established based on the opinions of the Committee. To further optimize these guidelines, periodic revision in line with the new evidence is necessary. [ABSTRACT FROM AUTHOR]

Published
2019
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211. The identification of autoantigens in mucous membrane pemphigoid using immortalized oral mucosal keratinocytes.

Author

Kamaguchi, Mayumi, Iwata, Hiroaki, Miyauchi, Toshinari, Ujiie, Hideyuki, Ujiie, Inkin, Nomura, Toshifumi, Ohga, Noritaka, Shimizu, Hiroshi, and Kitagawa, Yoshimasa

Subjects
MUCOUS membranes, PEMPHIGOID gestationis, ORAL mucosa, KERATINOCYTES, AUTOIMMUNE diseases, CHRONIC diseases
Abstract

Background: Mucous membrane pemphigoid (MMP) is a rare chronic autoimmune subepithelial blistering disorder, targeting multiple basement membrane zone (BMZ) proteins including collagen XVII (COL17). Circulating autoantibodies of MMP are often undetected due to their lower titers. The oral mucosa is a valuable substrate for the detection of autoantibodies in MMP patients. However, obtaining normal human oral mucosa is more difficult than obtaining normal human skin. We established immortalized normal human oral mucosal keratinocytes (OMKs) and performed immunoblotting using immortalized OMK lysate for detecting autoantigens in MMP.Methods: Immortalized OMKs were generated from primary OMKs using E6/E7 proteins of HPV. We compared the protein expression levels of major BMZ proteins between primary OMKs and immortalized OMKs. We performed immunoblotting to detect autoantigens using cell lysates from immortalized OMKs in 30 MMP patients.Results: There were no significant differences between primary OMKs and immortalized OMKs in terms of protein expression levels of the BMZ proteins, including COL17, laminin 332, integrin α6/β4, collagen VII, and collagen IV. Cell lysates of immortalized OMKs effectively identified MMP autoantigens in 60% (18/30) of MMP sera. We found an interesting case of MMP whose autoantibodies preferentially reacted to the 120-kD protein that is an ectodomain of COL17.Conclusion: We demonstrated that a cell lysate of immortalized OMKs is a reliable substrate for the detection of MMP autoantigens. This newly developed immunoblotting analysis method promises to contribute to the diagnosis of MMP. [ABSTRACT FROM AUTHOR]

Published
2019
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212. Type XVII Collagen–Specific CD4+T Cells Induce Bullous Pemphigoid by Producing IL-5

Author

Yoshimoto, Norihiro, Muramastsu, Ken, Ito, Takamasa, Zheng, Miao, Izumi, Kentaro, Natsuga, Ken, Iwata, Hiroaki, Hasegawa, Yoshinori, and Ujiie, Hideyuki

Abstract

Bullous pemphigoid is an autoimmune subepidermal blistering disease caused by anti–type XVII collagen (COL17) antibodies. Bullous pemphigoid has some immunological features such as eosinophilic infiltration and the deposition of IgE autoantibodies in the skin; however, the mechanism behind such features remains largely unclear. We focused on the autoantigen-specific CD4+T cells, which are considered to regulate immune response. We established COL17-specific CD4+T cell lines in vitro. Wild-type mice were immunized with synthesized peptides that include a pathogenic epitope of COL17, and lymphocytes were subjected to a limiting dilution assay. We established 5 T cell lines and examined the pathogenicity by transferring them with COL17-primed B cells into Rag-2−/−/COL17-humanized mice that express human COL17 but not mouse COL17 in the skin. Notably, 3 lines induced bullous pemphigoid–like skin changes associated with subepidermal separation and eosinophilic infiltration histologically and the production of anti-COL17 antibodies. The other 2 lines did not induce such phenotypes. RNA-sequencing analysis revealed that T helper 2 cytokines, particularly IL-5, were highly expressed in the pathogenic T-cell lines. Anti–IL-5 antibody administration significantly reduced the skin changes and attenuated the production of autoantibodies. Thus, the production of IL-5 is critical for COL17-specific CD4+T cells to induce bullous pemphigoid phenotypes in vivo.

Published
2024
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213. Autoantibody profile differentiates between inflammatory and noninflammatory bullous pemphigoid

Author

1000050793668, Izumi, Kentaro, 1000020443955, Nishie, Wataru, Mai, Yosuke, Wada, Mayumi, 1000070645457, Natsuga, Ken, 1000060374435, Ujiie, Hideyuki, 1000020397334, Iwata, Hiroaki, 1000080327618, Yamagami, Jun, 1000000146672, Shimizu, Hiroshi, 1000050793668, Izumi, Kentaro, 1000020443955, Nishie, Wataru, Mai, Yosuke, Wada, Mayumi, 1000070645457, Natsuga, Ken, 1000060374435, Ujiie, Hideyuki, 1000020397334, Iwata, Hiroaki, 1000080327618, Yamagami, Jun, 1000000146672, and Shimizu, Hiroshi

Abstract

Bullous pemphigoid (BP) is a major autoimmune blistering skin disorder, in which a majority of the autoantibodies (autoAbs) target the juxtamembranous extracellular noncollagenous 16A domain (NC16A) domain of hemidesmosomal collagen XVII. BP-autoAbs may target regions of collagen XVII other than the NC16A domain; however, correlations between epitopes of BP-autoAbs and clinical features have not been fully elucidated. To address correlations between the clinical features and specific epitopes of BP-autoAbs, we evaluated the epitope profiles of BP-autoAbs in 121 patients. A total of 87 patients showed a typical inflammatory phenotype with erythema and autoAbs targeting the anti-NC16A domain, whereas 14 patients showed a distinct noninflammatory phenotype, in which autoAbs specifically targeted the midportion of collagen XVII, but not NC16A. Interestingly, this group clinically showed significantly reduced erythema associated with scant lesional infiltration of eosinophils. Surprisingly, 7 of the 14 cases (50.0%) received dipeptidyl peptidase-IV inhibitors for the treatment of diabetes. Dipeptidyl peptidase-IV inhibitors were used in 3 of 76 (3.9%) typical cases of BP with autoAbs targeting NC16A; thus, dipeptidyl peptidase-IV inhibitors are thought to be involved in the development of atypical noninflammatory BP. This study shows that the autoAb profile differentiates between inflammatory and noninflammatory BP, and that noninflammatory BP may be associated with dipeptidyl peptidase-IV inhibitors.

Published
2016

214. A case of mucous membrane pemphigoid with anti‐BP230 autoantibodies alone.

Author

Yoshimoto, Norihiro, Ujiie, Inkin, Inamura, Emi, Natsuga, Ken, Nishie, Wataru, Shimizu, Hiroshi, and Ujiie, Hideyuki

Subjects
MUCOUS membranes, AUTOANTIBODIES, BULLOUS pemphigoid, EPIDERMOLYSIS bullosa
Abstract

Dear Editor, The mucous membrane pemphigoid (MMP) subtype of pemphigoid is a subepithelial blistering disease predominantly affecting the mucous membranes.1 The target antigens of MMP autoantibodies are components of the basement membrane zone (BMZ), such as BP180, BP230, laminin 332, integrin 4, and type VII collagen. However, the serum anti-BP230 IgG autoantibody titer was elevated as determined by ELISA (index value: 55.08; cutoff: <9). In BP, it is known that cases of BP with BP230 autoantibodies alone present with milder disease than classic BP,5 which is consistent with the favorable clinical course of the present case of MMP with BP230 autoantibodies alone. [Extracted from the article]

Published
2021
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224. Context-Dependent Regulation of Collagen XVII Ectodomain Shedding in Skin

Author

Nishie, Wataru, Natsuga, Ken, Iwata, Hiroaki, Izumi, Kentaro, Ujiie, Hideyuki, Toyonaga, Ellen, Hata, Hiroo, Nakamura, Hideki, Shimizu, Hiroshi, Nishie, Wataru, Natsuga, Ken, Iwata, Hiroaki, Izumi, Kentaro, Ujiie, Hideyuki, Toyonaga, Ellen, Hata, Hiroo, Nakamura, Hideki, and Shimizu, Hiroshi

Abstract

Pemphigoid is a common autoimmune blistering disorder in which autoantibodies target transmembrane collagen XVII (COL17), a component of hemidesmosomes in basal keratinocytes. The ectodomain of COL17 can be cleaved from the cell surface within the juxtamembranous extracellular NC16A domain, and, interestingly, certain autoantibodies of pemphigoid patients preferentially react with the shed ectodomain. These findings suggest that COL17 ectodomain shedding generates neoepitopes on the shed form; however, the regulatory mechanism of the shedding in in vivo skin and the pathogenicity of the neoepitope-targeting antibodies still are uncertain. To address these issues, we produced rabbit antibodies specifically reacting with N-terminal cleavage sites of the shed COL17 ectodomain. The antibodies showed that certain amounts of the human COL17 ectodomain are cleaved physiologically at Gln(525) in in vivo skin. In contrast, migrating human keratinocytes cleave COL17 at Leu(524) but not at Gln(525). The passive transfer of antibodies reacting with an N-terminal cleavage site of the mouse COL17 ectodomain into neonatal wild-type mice failed to induce blister formation, even though the antibodies bound to the dermal-epidermal junctions, indicating that cleavage site-specific antibodies have reduced or absent pathogenicity for blister formation. This study shows the ectodomain shedding of COL17 to be a physiological event in in vivo human skin that probably generates nonpathologic epitopes on the cleavage sites.

Published
2015

225. Context-Dependent Regulation of Collagen XVII Ectodomain Shedding in Skin

Author

1000020443955, Nishie, Wataru, Natsuga, Ken, Iwata, Hiroaki, Izumi, Kentaro, 1000060374435, Ujiie, Hideyuki, Toyonaga, Ellen, 1000090399915, Hata, Hiroo, 1000060435956, Nakamura, Hideki, 1000000146672, Shimizu, Hiroshi, 1000020443955, Nishie, Wataru, Natsuga, Ken, Iwata, Hiroaki, Izumi, Kentaro, 1000060374435, Ujiie, Hideyuki, Toyonaga, Ellen, 1000090399915, Hata, Hiroo, 1000060435956, Nakamura, Hideki, 1000000146672, and Shimizu, Hiroshi

Abstract

Pemphigoid is a common autoimmune blistering disorder in which autoantibodies target transmembrane collagen XVII (COL17), a component of hemidesmosomes in basal keratinocytes. The ectodomain of COL17 can be cleaved from the cell surface within the juxtamembranous extracellular NC16A domain, and, interestingly, certain autoantibodies of pemphigoid patients preferentially react with the shed ectodomain. These findings suggest that COL17 ectodomain shedding generates neoepitopes on the shed form; however, the regulatory mechanism of the shedding in in vivo skin and the pathogenicity of the neoepitope-targeting antibodies still are uncertain. To address these issues, we produced rabbit antibodies specifically reacting with N-terminal cleavage sites of the shed COL17 ectodomain. The antibodies showed that certain amounts of the human COL17 ectodomain are cleaved physiologically at Gln(525) in in vivo skin. In contrast, migrating human keratinocytes cleave COL17 at Leu(524) but not at Gln(525). The passive transfer of antibodies reacting with an N-terminal cleavage site of the mouse COL17 ectodomain into neonatal wild-type mice failed to induce blister formation, even though the antibodies bound to the dermal-epidermal junctions, indicating that cleavage site-specific antibodies have reduced or absent pathogenicity for blister formation. This study shows the ectodomain shedding of COL17 to be a physiological event in in vivo human skin that probably generates nonpathologic epitopes on the cleavage sites.

Published
2015

226. The direct binding of collagen XVII and collagen IV is disrupted by pemphigoid autoantibodies

Author

Kamaguchi, Mayumi, Iwata, Hiroaki, Nishie, Wataru, Toyonaga, Ellen, Ujiie, Hideyuki, Natsuga, Ken, Kitagawa, Yoshimasa, and Shimizu, Hiroshi

Abstract

The basement membrane zone (BMZ) is framed by hemidesmosomes and extracellular matrix (ECM) including collagen IV (COL4). Hemidesmosomes are multiprotein complexes that include collagen XVII (COL17). BMZ proteins can be targeted in autoimmune subepidermal blistering diseases, e.g., pemphigoid targeting COL17. The blistering mechanisms in pemphigoid have not been fully elucidated, especially in mucous membrane pemphigoid (MMP), which mainly affects the mucosa. In this study, we showed that oral lesions in pemphigoid may be attributed to the inhibition of protein–protein interactions by autoantibodies. Using immunoprecipitation, we revealed that COL17 directly binds to COL4 in normal human keratinocytes and normal human oral keratinocytes. In particular, the C-terminus of COL17 is binding site to COL4 in oral keratinocytes. The precise COL4-binding region on COL17 was determined by protein–protein binding assay to be from amino acid Gly1175to Asp1340on the C-terminus. MMP-IgG or mAb recognizing the C-terminus hindered the interaction of COL17 with COL4 in oral keratinocytes. Furthermore, keratinocyte adhesion strength to COL4-coated plates was significantly reduced by the treatment of mAb against the C-terminus. In addition, the inflammatory infiltrates around perilesions were significantly less in MMP compared to BP. These results indicate that pemphigoid IgG targeting the C-terminus plays a pathogenic role in blister formation in the oral mucosa to inhibit protein interactions with less inflammation.

Published
2019
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228. A case of atopic dermatitis‐associated dupilumab‐resistant alopecia totalis successfully treated with baricitinib.

Author

Seo, Takashi, Izumi, Kentaro, Kawamura, Takuya, Tsujiwaki, Masumi, and Ujiie, Hideyuki

Subjects
ALOPECIA areata, BARICITINIB, TREATMENT effectiveness, BALDNESS
Abstract

Improvement of severe AD-associated AA with the administration of baricitinib, a JAK 1/2 inhibitor, or dupilumab has been reported.[[3]] We report a case of severe refractory AA complicated by AD successfully treated by switching from dupilumab to baricitinib. Atopic dermatitis (AD) is a chronic inflammatory skin disease that is characterized by intense itching and recurrent eczematous lesions.[1] Systemic treatments such as dupilumab, Janus kinase (JAK) inhibitors, and immunosuppressive agents are considered for patients with moderate to severe disease unresponsive to topical therapies. AD is a well-known complication of alopecia areata (AA).[2] AA is recurrent and refractory in certain cases, with limited treatment options. [Extracted from the article]

Published
2022
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229. Autoantibodies to Multiple Epitopes on the Non-Collagenous-1 Domain of Type VII Collagen Induce Blisters

Author

Vorobyev, Artem, primary, Ujiie, Hideyuki, additional, Recke, Andreas, additional, Buijsrogge, Jacqueline J.A., additional, Jonkman, Marcel F., additional, Pas, Hendri H., additional, Iwata, Hiroaki, additional, Hashimoto, Takashi, additional, Kim, Soo-Chan, additional, Hoon Kim, Jong, additional, Groves, Richard, additional, Samavedam, Unni, additional, Gupta, Yask, additional, Schmidt, Enno, additional, Zillikens, Detlef, additional, Shimizu, Hiroshi, additional, and Ludwig, Ralf J., additional

Published
2015
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237. Complement-independent blistering mechanisms in bullous pemphigoid.

Author

Iwata, Hiroaki and Ujiie, Hideyuki

Subjects
*AUTOIMMUNE diseases, *SKIN diseases, *CYTOKINES, *COLLAGEN, *PATHOGENIC microorganisms
Abstract

Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease that clinically demonstrates tense blisters with widespread erythema, histologically demonstrates subepidermal blistering and immunologically demonstrates the presence of circulating autoantibodies against hemidesmosomal molecules. Complement activation has long been regarded as necessary for the generation of the BP. However, certain evidence has recently come to support non-complemental blistering mechanisms. The story of BP blistering mechanisms is a complicated one. This review mainly focuses on a specific blistering mechanism that highlights the role of complements in BP blistering. [ABSTRACT FROM AUTHOR]

Published
2017
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238. Autoantibodies of non-inflammatory bullous pemphigoid hardly deplete type XVII collagen of keratinocytes.

Author

Imafuku, Keisuke, Iwata, Hiroaki, Kamaguchi, Mayumi, Izumi, Kentaro, Natsuga, Ken, Ujiie, Hideyuki, Nishie, Wataru, and Shimizu, Hiroshi

Subjects
COLLAGEN, PHYSIOLOGICAL control systems, BULLOUS pemphigoid, BLOOD viscosity, BLOOD hyperviscosity syndrome
Abstract

Type XVII collagen ( COL17) and the non-collagenous 16A ( NC16A) domain is regarded as the major pathogenic domains for bullous pemphigoid ( BP). Some patients with BP have autoantibodies against parts of COL17 outside the NC16A domain (hereinafter the non- NC16A domain) and show less inflammatory manifestations. There were no significant differences in titres and IgG subclasses between NC16A- BP and non- NC16A- BP as determined by indirect immunofluorescent microscopy. The neutrophil activation capacities determined by ROS release did not differ between NC16A- BP and non- NC16A- BP. However, NC16A- BP IgG depleted COL17 in a dose-dependent manner. Treatment with NC16A- BP IgG, but not with non- NC16A- BP IgG, significantly decreased the adhesion strength. We speculate that the differences in clinical severity between NC16A- BP and non- NC16A- BP relate to the degree of COL17 depletion. [ABSTRACT FROM AUTHOR]

Published
2017
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243. Paper-Based ELISA for the Detection of Autoimmune Antibodies in Body Fluid—The Case of Bullous Pemphigoid

Author

Hsu, Chao-Kai, primary, Huang, Hsin-Yu, additional, Chen, Wan-Rung, additional, Nishie, Wataru, additional, Ujiie, Hideyuki, additional, Natsuga, Ken, additional, Fan, Shu-Ting, additional, Wang, Hsi-Kai, additional, Lee, Julia Yu-Yun, additional, Tsai, Wei-Lun, additional, Shimizu, Hiroshi, additional, and Cheng, Chao-Min, additional

Published
2014
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244. High Expression of Collagen XVII Compensates for its Depletion Induced by Pemphigoid IgG in the Oral Mucosa

Author

Kamaguchi, Mayumi, Iwata, Hiroaki, Ujiie, Hideyuki, Natsuga, Ken, Nishie, Wataru, Kitagawa, Yoshimasa, and Shimizu, Hiroshi

Abstract

The basement membrane zone consists of multiple components, including collagen XVII (COL17), which is the target of bullous pemphigoid. To our knowledge, no research has addressed the differences in basement membrane zone components between the skin and oral mucosa; therefore, we investigated the basement membrane zone proteins, with a focus on COL17. The mRNA and protein expression levels of COL17 were significantly higher in oral keratinocytes than in skin keratinocytes. Hemidesmosomal COL17 expression was markedly higher in oral keratinocytes than in skin keratinocytes, and its level was associated with adhesion strength. Oral keratinocytes adhered to the extracellular matrix more tightly than did skin keratinocytes in vitro. Based on these results, we attempt to explain the clinical diversity of bullous pemphigoid. COL17 depletion was more prominent in skin keratinocytes than in oral keratinocytes after treatment with COL17-NC16A mAbs, which have in vivo pathogenicity. COL17 C-terminus mAbs, which are not pathogenic, facilitated COL17 depletion in combination treatment with COL17-NC16A mAbs in both types of keratinocytes. In summary, the greater amount of COL17 in oral keratinocytes than in skin keratinocytes is associated with the higher strength of oral keratinocyte hemidesmosomal adhesion at the basement membrane zone. Our results may explain why bullous pemphigoid blistering tends to be more prevalent in the skin than in the oral mucosa.

Published
2018
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245. Intravenous IgG Reduces Pathogenic Autoantibodies, Serum IL-6 Levels, and Disease Severity in Experimental Bullous Pemphigoid Models

Author

Sasaoka, Tetsumasa, Ujiie, Hideyuki, Nishie, Wataru, Iwata, Hiroaki, Ishikawa, Makoto, Higashino, Hiroshi, Natsuga, Ken, Shinkuma, Satoru, and Shimizu, Hiroshi

Abstract

Bullous pemphigoid (BP) is an autoimmune blistering disease characterized by autoantibodies to COL17. Currently, systemic corticosteroids are used as first-line treatments for BP; alternatively, intravenous administration of high-dose IgG (IVIG) has been shown to be effective for patients with steroid-resistant BP in clinical practice. However, the effect of IVIG on BP has not fully been investigated. To examine the effects and mechanisms of action of IVIG against BP, we performed IVIG experiments using two experimental BP mouse models. One is a passive-transfer BP model that reproduces subepidermal separation in neonatal mice by the passive transfer of IgGs against COL17, such as polyclonal or monoclonal mouse IgG or IgG from BP patients. The other is an active BP model that continuously develops a disease phenotype in adult mice. IVIG decreased pathogenic IgG and the disease scores in both models. Injected IVIG distributed throughout the dermis and the intercellular space of the lower epidermis. Notably, IVIG inhibited the increase of IL-6 in both models, possibly by suppressing the production of IL-6 by keratinocytes. These results suggest that the inhibitory effects of IVIG on BP are associated with the reduction of pathogenic IgG and the modulation of cytokine production.

Published
2018
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247. Coexistence case of bullous pemphigoid and pemphigus foliaceus

Author

Tsujiwaki, Masumi, additional, Abe, Riichiro, additional, Nomura, Yukiko, additional, Nishimura, Machiko, additional, Hoshina, Daichi, additional, Shinkuma, Satoru, additional, Natsuga, Ken, additional, Ujiie, Hideyuki, additional, Arita, Ken, additional, and Shimizu, Hiroshi, additional

Published
2013
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