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Antibodies
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Advances in the Use of Therapeutic Antibodies and Identification of...
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Advances in the Use of Therapeutic Antibodies and Identification of Novel Autoantibodies in Dermatologic Disease

A special issue of Antibodies (ISSN 2073-4468).

Deadline for manuscript submissions: closed (15 July 2022) | Viewed by 16164

Special Issue Editor

Dr. Kyle T. Amber

E-Mail Website
Guest Editor
1. Rush University Medical Center, Division of Dermatology, Department of Otorhinolaryngology—Head and Neck Surgery, Rush University, Chicago, IL 60612, USA
2. Rush University Medical Center, Department of Internal Medicine, Rush University, Chicago, IL 60612, USA
Interests: autoimmune blistering disease; immune–epidermal interactions; mitigating steroid induced comorbidities; autoimmune blistering diseases; dermatology; atopic dermatitis; dermatomyositis; cutaneous lymphoma; psoriasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent technologies have led to the development of numerous therapeutic antibodies in the treatment of dermatologic diseases, as well as the identification of novel circulating autoantibodies. In this Special Issue, we will cover novel therapeutic antibodies, as well as newly identified autoantibodies that may be pathogenic or serve as a biomarker in cutaneous disease.

Dr. Kyle T. Amber
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antibodies is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Atopic Dermatitis
  • Psoriasis
  • Dermatomyositis
  • Autoimmune Blistering Disease
  • Palmar Plantar Pustulosis
  • Generalized Pustular Psoriasis
  • Pemphigus
  • Pemphigoid
  • Epidermolysis Bullosa Acquisita
  • Lupus Erythematosus
  • Morphea
  • Sclerodema
  • Chronic Idiopathic Urticaria
  • Dermatology

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Published Papers (3 papers)

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Review

8 pages, 489 KiB  
Review
Mitochondrial Autoantibodies and the Role of Apoptosis in Pemphigus Vulgaris
by Dana M. Hutchison, Anna-Marie Hosking, Ellen M. Hong and Sergei A. Grando
Antibodies 2022, 11(3), 55; https://doi.org/10.3390/antib11030055 - 25 Aug 2022
Cited by 5 | Viewed by 4082
Abstract
Pemphigus vulgaris (PV) is an IgG autoantibody-mediated, potentially fatal mucocutaneous disease manifested by progressive non-healing erosions and blisters. Beyond acting to inhibit adhesion molecules, PVIgGs elicit a unique process of programmed cell death and detachment of epidermal keratinocytes termed apoptolysis. Mitochondrial damage by [...] Read more.
Pemphigus vulgaris (PV) is an IgG autoantibody-mediated, potentially fatal mucocutaneous disease manifested by progressive non-healing erosions and blisters. Beyond acting to inhibit adhesion molecules, PVIgGs elicit a unique process of programmed cell death and detachment of epidermal keratinocytes termed apoptolysis. Mitochondrial damage by antimitochondrial antibodies (AMA) has proven to be a critical link in this process. AMA act synergistically with other autoantibodies in the pathogenesis of PV. Importantly, absorption of AMA inhibits the ability of PVIgGs to induce blisters. Pharmacologic agents that protect mitochondrial function offer a new targeted approach to treating this severe immunoblistering disease. Full article
(This article belongs to the Special Issue Advances in the Use of Therapeutic Antibodies and Identification of Novel Autoantibodies in Dermatologic Disease)
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11 pages, 561 KiB  
Review
Deciphering the Contribution of BP230 Autoantibodies in Bullous Pemphigoid
by Connor Cole, Luca Borradori and Kyle T. Amber
Antibodies 2022, 11(3), 44; https://doi.org/10.3390/antib11030044 - 28 Jun 2022
Cited by 6 | Viewed by 5418
Abstract
Bullous pemphigoid (BP) is a subepidermal autoimmune blistering disease predominantly affecting elderly patients and carries significant morbidity and mortality. Patients typically suffer from severe itch with eczematous lesions, urticarial plaques, and/or tense blisters. BP is characterized by the presence of circulating autoantibodies against [...] Read more.
Bullous pemphigoid (BP) is a subepidermal autoimmune blistering disease predominantly affecting elderly patients and carries significant morbidity and mortality. Patients typically suffer from severe itch with eczematous lesions, urticarial plaques, and/or tense blisters. BP is characterized by the presence of circulating autoantibodies against two components of the hemidesmosome, BP180 and BP230. The transmembrane BP180, also known as type XVII collagen or BPAG2, represents the primary pathogenic autoantigen in BP, whereas the intracellular BP230 autoantigen is thought to play a minor role in disease pathogenesis. Although experimental data exist suggesting that anti-BP230 antibodies are secondarily formed following initial tissue damage mediated by antibodies targeting extracellular antigenic regions of BP180, there is emerging evidence that anti-BP230 IgG autoantibodies alone directly contribute to tissue damage. It has been further claimed that a subset of patients has a milder variant of BP driven solely by anti-BP230 autoantibodies. Furthermore, the presence of anti-BP230 autoantibodies might correlate with distinct clinical features. This review summarizes the current understanding of the role of BP230 and anti-BP230 antibodies in BP pathogenesis. Full article
(This article belongs to the Special Issue Advances in the Use of Therapeutic Antibodies and Identification of Novel Autoantibodies in Dermatologic Disease)
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15 pages, 1317 KiB  
Review
A Review of Acquired Autoimmune Blistering Diseases in Inherited Epidermolysis Bullosa: Implications for the Future of Gene Therapy
by Payal M. Patel, Virginia A. Jones, Christy T. Behnam, Giovanni Di Zenzo and Kyle T. Amber
Antibodies 2021, 10(2), 19; https://doi.org/10.3390/antib10020019 - 17 May 2021
Cited by 8 | Viewed by 5358
Abstract
Gene therapy serves as a promising therapy in the pipeline for treatment of epidermolysis bullosa (EB). However, with great promise, the risk of autoimmunity must be considered. While EB is a group of inherited blistering disorders caused by mutations in various skin proteins, [...] Read more.
Gene therapy serves as a promising therapy in the pipeline for treatment of epidermolysis bullosa (EB). However, with great promise, the risk of autoimmunity must be considered. While EB is a group of inherited blistering disorders caused by mutations in various skin proteins, autoimmune blistering diseases (AIBD) have a similar clinical phenotype and are caused by autoantibodies targeting skin antigens. Often, AIBD and EB have the same protein targeted through antibody or mutation, respectively. Moreover, EB patients are also reported to carry anti-skin antibodies of questionable pathogenicity. It has been speculated that activation of autoimmunity is both a consequence and cause of further skin deterioration in EB due to a state of chronic inflammation. Herein, we review the factors that facilitate the initiation of autoimmune and inflammatory responses to help understand the pathogenesis and therapeutic implications of the overlap between EB and AIBD. These may also help explain whether corrections of highly immunogenic portions of protein through gene therapy confers a greater risk towards developing AIBD. Full article
(This article belongs to the Special Issue Advances in the Use of Therapeutic Antibodies and Identification of Novel Autoantibodies in Dermatologic Disease)
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