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      Bullous Pemphigoid: Trigger and Predisposing Factors

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          Abstract

          Bullous pemphigoid (BP) is the most frequent autoimmune subepidermal blistering disease provoked by autoantibodies directed against two hemidesmosomal proteins: BP180 and BP230. Its pathogenesis depends on the interaction between predisposing factors, such as human leukocyte antigen (HLA) genes, comorbidities, aging, and trigger factors. Several trigger factors, such as drugs, thermal or electrical burns, surgical procedures, trauma, ultraviolet irradiation, radiotherapy, chemical preparations, transplants, and infections may induce or exacerbate BP disease. Identification of predisposing and trigger factors can increase the understanding of BP pathogenesis. Furthermore, an accurate anamnesis focused on the recognition of a possible trigger factor can improve prognosis by promptly removing it.

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          International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).

          S Miyakis, M Lockshin, T Atsumi … (2006)
          New clinical, laboratory and experimental insights, since the 1999 publication of the Sapporo preliminary classification criteria for antiphospholipid syndrome (APS), had been addressed at a workshop in Sydney, Australia, before the Eleventh International Congress on antiphospholipid antibodies. In this document, we appraise the existing evidence on clinical and laboratory features of APS addressed during the forum. Based on this, we propose amendments to the Sapporo criteria. We also provide definitions on features of APS that were not included in the updated criteria.
          Article 0 comments Cited 847 times – based on 0 reviews     Review now
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            The PD-1 pathway in tolerance and autoimmunity.

            Loise Francisco, Peter Sage, Arlene Sharpe (2010)
            Regulatory T cells (Tregs) and the PD-1: PD-ligand (PD-L) pathway are both critical to terminating immune responses. Elimination of either can result in the breakdown of tolerance and the development of autoimmunity. The PD-1: PD-L pathway can thwart self-reactive T cells and protect against autoimmunity in many ways. In this review, we highlight how PD-1 and its ligands defend against potentially pathogenic self-reactive effector T cells by simultaneously harnessing two mechanisms of peripheral tolerance: (i) the promotion of Treg development and function and (ii) the direct inhibition of potentially pathogenic self-reactive T cells that have escaped into the periphery. Treg cells induced by the PD-1 pathway may also assist in maintaining immune homeostasis, keeping the threshold for T-cell activation high enough to safeguard against autoimmunity. PD-L1 expression on non-hematopoietic cells as well as hematopoietic cells endows PD-L1 with the capacity to promote Treg development and enhance Treg function in lymphoid organs and tissues that are targets of autoimmune attack. At sites where transforming growth factor-beta is present (e.g. sites of immune privilege or inflammation), PD-L1 may promote the de novo generation of Tregs. When considering the consequences of uncontrolled immunity, it would be therapeutically advantageous to manipulate Treg development and sustain Treg function. Thus, this review also discusses how the PD-1 pathway regulates a number of autoimmune diseases and the therapeutic potential of PD-1: PD-L modulation.
            Article 0 comments Cited 494 times – based on 0 reviews     Review now
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              Toll-like receptor 7 (TLR7)-driven accumulation of a novel CD11c⁺ B-cell population is important for the development of autoimmunity.

              Anatoly V Rubtsov, Kira Rubtsova, Aryeh Fischer … (2011)
              Females are more susceptible than males to many autoimmune diseases. The processes causing this phenomenon are incompletely understood. Here, we demonstrate that aged female mice acquire a previously uncharacterized population of B cells that we call age-associated B cells (ABCs) and that these cells express integrin α(X) chain (CD11c). This unexpected population also appears in young lupus-prone mice. On stimulation, CD11c(+) B cells, both from autoimmune-prone and healthy strains of mice, secrete autoantibodies, and depletion of these cells in vivo leads to reduction of autoreactive antibodies, suggesting that the cells might have a direct role in the development of autoimmunity. We have explored factors that contribute to appearance of ABCs and demonstrated that signaling through Toll-like receptor 7 is crucial for development of this B cell population. We were able to detect a similar population of B cells in the peripheral blood of some elderly women with autoimmune disease, suggesting that there may be parallels between the creation of ABC-like cells between mice and humans.
              Article 0 comments Cited 234 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biomolecules
                Journal ID (iso-abbrev): Biomolecules
                Journal ID (publisher-id): biomolecules
                Title: Biomolecules
                Publisher: MDPI
                ISSN (Electronic): 2218-273X
                Publication date (Electronic): 10 October 2020
                Publication date Collection: October 2020
                Volume: 10
                Issue: 10
                Electronic Location Identifier: 1432
                Affiliations
                First Dermatology Clinic, IDI-IRCCS, Via Dei Monti di Creta 104, 00167 Rome, Italy; jlsinagra@ 123456hotmail.com (J.L.M.S.); a.salemme@ 123456idi.it (A.S.); g.dizenzo@ 123456idi.it (G.D.Z.)
                Author notes
                [* ]Correspondence: f.moro@ 123456idi.it (F.M.); l.fania@ 123456idi.it (L.F.); Tel.: +39-(342)-802-0004 (F.M.)
                [†]

                These authors have equally contributed to the manuscript.

                Author information
                https://orcid.org/0000-0003-0031-941X
                Article
                Publisher ID: biomolecules-10-01432
                DOI: 10.3390/biom10101432
                PMC ID: 7600534
                PubMed ID: 33050407
                SO-VID: 30071899-6d7b-47e7-8dac-a52f546a7233
                Copyright © © 2020 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 07 September 2020
                Date accepted : 08 October 2020
                Categories
                Subject: Review

                Keywords: bullous pemphigoid,autoimmune bullous disease,trigger factors,predisposing factors,etiopathogenesis
                Data availability:
                Keywords: bullous pemphigoid, autoimmune bullous disease, trigger factors, predisposing factors, etiopathogenesis

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