BACKGROUND:Despite the established association between gliptins and bullous pemphigoid (BP), knowledge of BP risk and its clinical and immunological phenotypes among individual gliptins remains fragmentary. OBJECTIVE:To estimate BP risk among different gliptins, compare the demographic, clinical, and immunological profiles of idiopathic and patients with bullous pemphigoid and gliptin-treated type 2 diabetes (BPT2D-G), and evaluate the diagnostic performance of a BP180-ectodomain enzyme-linked immunosorbent assay. METHODS:Patients with BP and/or type 2 diabetes who visited 2 Italian hospitals during 2019 to 2023 were prospectively enrolled and clinically/immunologically characterized in a case-control study using in-house enzyme-linked immunosorbent assays detecting reactivity to BP180 extracellular epitopes. RESULTS:Overall, gliptin exposure demonstrated a strong association with BP, whereas sitagliptin did not exhibit a comparable effect. BPT2D-G showed a distinctive humoral profile, with high reactivity to other epitopes beyond BP180-noncollagenous 16A domain. A subset of patients, mainly exposed to linagliptin and BP180-noncollagenous 16A domain/BP230 negative, presented milder, often noninflammatory disease: a BP180-ectodomain assay improved diagnostic performances in these patients. LIMITATIONS:Potential residual confounding; limited generalizability; limited data on gliptin exposure duration. The observational design precludes causal inference. CONCLUSION:Different BP risks among gliptins may inform therapeutic choices, favoring sitagliptin in elderly patients. Personalized management of patients with BP180-noncollagenous 16A domain/BP230-negative BPT2D-G may reduce unnecessary use of high-potency topical and systemic corticosteroids. BP180-ectodomain-based diagnostic assays may facilitate BPT2D-G diagnosis.

Pemphigus is a life-threatening autoimmune blistering disease affecting skin and mucous membranes. Despite its etiopathogenesis remains largely unknown, several trigger and predisposing factors have been reported. Pemphigus is caused by autoantibodies that target desmoglein 1 and desmoglein 3, impacting desmosome function. However, circulating autoantibodies are often the consequence of a precipitating factor that occurs in predisposed individuals. This review aims to describe and discuss almost all trigger and predisposing factors reported as possible or probable cause of the disease. Among the reported trigger factors that may induce or exacerbate pemphigus, we have found of particular interest: drug intake (especially thiol- and phenol-containing compounds), vaccines, infections, as well as some reports about pregnancy, radiations, emotional stress, pesticides and physical trauma. Moreover, we discuss the possible role of food intake in pemphigus onset and particular attention is given to dietary factors containing thiol, phenol and tannin compounds. A trigger factor is “the straw that breaks the camel’s back,” and often acts together with predisposing factors. Here we discuss how pemphigus onset may be influenced by genetic susceptibility and comorbidities like thyroid diseases, malignancies and other autoimmune disorders.To identify other hitherto unknown trigger and predisposing factors, well designed prospective studies are needed. In this context, future research should explore their connection with the aim to advance our understanding of pemphigus pathogenesis.

Bullous pemphigoid (BP) is an autoimmune blistering disease that targets the haemidesmosomal proteins, mainly BP180. Extracellular vesicles (EVs) have been demonstrated to carry tissue-specific autoantigens in the setting of autoimmune diseases and transplant organ rejection; this phenomenon was demonstrated to have pathogenic implications in autoimmune diseases and to correlate with transplant rejection severity. The purpose of this study was to identify the presence of BP targeted autoantigens in blister fluid derived EVs. We isolated, by size exclusion chromatography, EVs derived from blisters of BP-patients and from suction blisters of healthy donors. EV characterization was performed by flow cytometry and nanoparticle tracking analysis. Western blot analysis was used to investigate the presence of autoantigens. A suspension enriched in EVs was efficiently obtained from blister fluid from patients and healthy donors. EV-enriched fractions were enriched in particles with a size distribution characterizing small-EVs (main peak was present at 94.5 nm). BP180 was found, by western blot analysis, in EVs derived from blister fluid of 3 out 6 BP patients and in none of EVs isolated from suction blister fluid of healthy donors. BP230 and Dsg1 were not detectable in EVs of any of the samples. No specific clinical characteristics seemed to correlate to the presence of BP180 in EVs. The discovery of BP180 in EVs derived from blister fluid might help understanding BP pathogenesis.

Background Mucous membrane pemphigoid (MMP) with anti-laminin 332 autoantibodies may be associated with malignancies, however, current serological assays have considerable limitations. At present, no commercial test for anti-laminin 332 antibodies is available, restricting the diagnosis to specialized laboratories worldwide. Biochip immunofluorescence microscopy has shown promising results in selected cohorts of laminin 332-MMP patients. Objectives To detect anti-laminin 332 antibodies by biochip immunofluorescence microscopy in a real-life cohort of MMP patients and compare the results with those from traditional immunoblotting. Materials & Methods Sera were obtained from 31 patients with MMP, 28 with bullous pemphigoid, five with pemphigus vulgaris, five with paraneoplastic pemphigus, five with linear IgA bullous dermatosis, and 10 controls, and analysed by biochip immunofluorescence using human cells expressing laminin 332. Immunoblotting was performed using purified laminin 332. Results MMP involved the oral mucosa in 65%, ocular mucosa in 9%, oral and ocular mucosae extensively in 13% as well as other mucosae in 13% of patients. Concomitant cutaneous involvement was reported in 35% of patients. Three MMP patients had an underlying malignancy. Anti-laminin 332 antibodies were detected in 2/31 (6%) cases by both methods. Based on immunoblotting, both laminin 332-positive sera reacted with α3 chain (in one case also with β3 chain). Both patients with anti-laminin 332 antibodies had extensive mucosal involvement and only one had cancer. Anti-laminin 332 antibodies were not detected in control groups. Conclusion Biochip immunofluorescence is an appropriate technique to detect anti-laminin 332 antibodies which should be tested in patients with MMP.

Bullous pemphigoid (BP) is an autoimmune bullous disease, characterized by autoantibodies targeting BP180 and BP230. The role of interleukin (IL)‐36, a potent chemoattractant for granulocytes, in BP remains elusive.The expression of IL‐36 cytokines (IL‐36α, β, γ) and their antagonists (IL‐36Ra and IL‐38) was analysed in the skin and serum samples of patients with BP (n = 31), psoriasis (n = 10) and healthy controls (HC) (n = 14) by quantitative polymerase chain reaction and enzyme linked immunosorbent assay, respectively. Skin and serum levels of all cytokines were correlated with the Bullous Pemphigoid Disease Area Index (BPDAI) score and with the serum concentration of pathogenic antibodies.IL‐36α, IL‐36β, IL‐36γ and IL‐36Ra were significantly (p < 0.05) overexpressed in BP skin compared to HC, without remarkable differences relative to psoriasis skin. The expression of IL‐38 was significantly (p < 0.05) higher in BP compared to psoriasis skin.IL‐36α and γ, but not β, serum concentrations were significantly (p < 0.05) higher in BP compared to HC. IL‐36γ was significantly (p < 0.05) more expressed in the serum of psoriasis patients than BP. The serum concentration of IL‐36Ra and IL‐38 were similar between BP and HC, while IL‐38 serum levels were significantly (p < 0.05) higher in BP compared to psoriasis patients. Serum IL‐36α correlated significantly with BPDAI (r = 0.5 p = 0.001).IL‐36 agonists are increased in BP patients, both locally and systemically. Serum IL‐36α might represent a potential biomarker for BP. An inefficient balance between IL‐36 agonists and antagonists is likely to occur during BP inflammation.

Abstract Bullous pemphigoid (BP) is an autoimmune blistering disease that targets the haemidesmosomal proteins, mainly BP180. Extracellular vesicles (EVs) have been demonstrated to carry tissue-specific autoantigens in the setting of autoimmune diseases and transplant organ rejection; this phenomenon was demonstrated to have pathogenic implications in autoimmune diseases and to correlate with transplant rejection severity. The purpose of this study was to identify the presence of BP targeted autoantigens in blister fluid derived EVs. We isolated, by size exclusion chromatography, EVs derived from blisters of BP-patients and from suction blisters of healthy donors. EV characterization was performed by flow cytometry and nanoparticle tracking analysis. Western blot analysis was used to investigate the presence of autoantigens. A suspension enriched in EVs was efficiently obtained from blister fluid from patients and healthy donors. EV-enriched fractions were enriched in particles with a size distribution characterizing small-EVs (main peak was present at 94.5nm). BP180 was found, by western blot analysis, in EVs derived from blister fluid of 3 out 6 BP patients and in none of EVs isolated from suction blister fluid of healthy donors. BP230 and Dsg1 were not detectable in EVs of any of the samples. No specific clinical characteristics seemed to correlate to the presence of BP180 in EVs. The discovery of BP180, the most important autoantigen targeted in BP, in EVs derived from blister fluid represent a milestone in the understanding of BP pathogenesis.

Background: Recently, several case-control studies demonstrated an association between gliptins and bullous pemphigoid (BP) occurrence. However, data on the clinical and immunologic features of gliptinassociated bullous pemphigoid (GABP) are controversial.Objective: This study aimed to clinically and immunologically characterize a large cohort of GABP patients to get an insight into the pathophysiology of this emerging drug-induced variant of BP.Methods: Seventy-four GABP patients were prospectively enrolled and characterized from 9 different Italian dermatology units between 2013 and 2020.Results: Our findings demonstrated the following in the GABP patients: (1) a noninflammatory phenotype, which is characterized by low amounts of circulating and skin-infiltrating eosinophils, is frequently found; (2) immunoglobulin (Ig)G, IgE, and IgA humoral responses to BP180 and BP230 antigens are reduced in frequency and titers compared with those in patients with idiopathic BP; (3) IgG reactivity targets multiple BP180 epitopes other than noncollagenous region 16A.Limitations: A limitation of the study is that the control group did not comprise only type 2 diabetes mellitus patients with BP.Conclusion: GABP patients show peculiar features of anti-BP180 and-BP230 humoral responses, laying the foundation for diagnostic improvements and getting novel insights into understanding the mechanism of BP onset. ( J Am Acad Dermatol 2022;87:56-63.)

BackgroundPemphigus vulgaris is an autoimmune intraepithelial bullous disease involving the skin and the mucous membranes. Imiquimod, a topical therapy for skin basal cell carcinoma, is an amine that induces the production of tumor necrosis factor alfa, interleukin-1 and other cytokines. Pemphigus induced by drugs has been frequently reported, mostly after systemic therapy.Case presentationWe present the case of a 50-year-old man who developed skin, intraoral, and genital mucosae lesions 3 days after a treatment with Imiquimod for multiple superficial basal cell carcinoma of the trunk. Direct and indirect immunofluorescence results were compatible with the diagnosis of pemphigus vulgaris. Enzyme-linked immunosorbent assay was negative for desmoglein 1 and 3, but interestingly, by immunoblotting on keratinocyte extracts a band of 170 kDa was obtained by IgG. The patient, after interrupting Imiquimod application, started a treatment with prednisolone and in 4 weeks showed a complete remission.ConclusionTopical Imiquimod therapy might induce atypical pemphigus vulgaris in some patients.

Anti-p200 pemphigoid is a rare subset of the pemphigoid group, in which the target antigen corresponds to laminin-γ1, a 200 kDa protein located within the lower lamina lucida of the basement membrane zone (BMZ).1 An 89-year-old Caucasian man presented with a 2-month history of a widespread cutaneous eruption associated with a modest itch. Physical examination showed blisters and erosions, some of them covered by scales and crusts, located at limbs and trunk (Fig. 1). Histopathology revealed hyper orthokeratosis and a mild perivascular inflammatory infiltration composed of lymphocytes and eosinophils. Direct immunofluorescence (DIF) of perilesional skin showed linear deposition of immunoglobulin (Ig) G and C3 along the BMZ. Serration pattern analysis was consistent with a pattern that resembled more an inverted “u,” rather than an “n.” DIF on salt split skin (SSS) revealed dermal deposition of IgG and C3. Indirect immunofluorescence (IIF) on SSS showed linear IgG deposition at the dermal side of BMZ. BIOCHIP™ for laminin-332 gave negative results. An enzyme-linked immunosorbent assay (ELISA) for antibodies against BP180, BP230 (MBL, Woburn, MA, USA), and type VII collagen (Euroimmun, Lübeck, Germany) was negative. Immunoblotting (IB) using recombinant laminin-421 revealed a weak IgG positivity and confirmed the absence of antibodies against BP180, BP230, and LAD antigens. A diagnosis of anti-p200 pemphigoid was eventually made. The patient was treated with oral (deflazacort 0.5 mg/kg/die) and topical corticosteroids. Remission was achieved by 5 months of treatment, and no recurrences were observed after 2-year follow-up. Diagnosis of anti-p200 pemphigoid is challenging. Clinical presentation resembles that of other pemphigoids, while standardized methods to detect circulating IgG targeting laminin-γ1, for example ELISA, are not available.2 Suspicion arises when linear antibody deposition along the dermal side of the BMZ is observed, and there is no evidence of anti-COL7 and anti-laminin-332 antibodies at serum tests. Recently, an IB method for diagnosing anti-p200 pemphigoid has been proposed by Solimani and was used in this case to confirm the diagnosis. The method consists of a two-step IB analysis, evaluating laminin-111 and laminin-421 reactivity first, followed by laminin-γ1 monomer in case of no previous reactivity.3 Serration pattern analysis provides a useful tool for the differential diagnosis of pemphigoids. The u-serrated pattern is highly specific for the diagnosis of epidermolysis bullosa acquisita, while the n-serrated pattern is typically observed in bullous pemphigoid.4 In literature, 13 cases of p200-pemphigoids were analyzed by serration pattern analysis: 11 patients (84.6%) were interpreted as n-serrated, while two (15.4%) showed an undetermined pattern.1 Our case was consistent neither with an n- nor with a u-serrated pattern but rather with a ‘u-inverted’ pattern, which has not been reported in the literature so far. Interestingly, immune electron microscopy in anti-p200 pemphigoid suggests that immune deposits are localized to the indentation of the non-hemidesmosomal portion of the lower lamina lucida which seems to be consistent with the morphology of the IgG deposition at the serration analysis in this case (Fig. 2).5 Anti-p200 pemphigoid is characterized by a more benign course than other pemphigoids, and thereby its treatment should rely on less invasive strategies.2 Although further cases are required to confirm our hypothesis, the inverted-U pattern might provide a clue for making the diagnosis of anti-p200 pemphigoid by DIF.

Pemphigus vulgaris is an intraepidermal autoimmune mucocutaneous blistering disease whose etiopathogenesis includes various trigger factors, i.e., drugs and malignancies. We present a case of malignancy-exacerbated pemphigus vulgaris which required a careful diagnostic process in order to rule out paraneoplastic pemphigus, along with the challenges posed by the need of treating both cutaneous and oncologic diseases. Possible post-operative complications post-poned the start of first-line immunosuppressive treatment of pemphigus. Moreover, the infective risks had to be minimized during the peak of the COVID-19 pandemic in Italy. Intravenous immunoglobulins were chosen as “bridge” therapy before the tumor surgical excision, followed by rituximab in post-operative phase.

COVID-19 is characterized by a severe pulmonary disease due to severe acute respiratory syndrome (SARS)-CoV-2 infection. For clinicians involved in the management of patients with chronic autoimmune diseases the risk linked to the conditions itself and to drug-induced immunosuppression during the COVID-19 pandemic is a major topic. Pemphigus is a rare autoimmune blistering disease (AIBD) of the skin and mucous membranes caused by autoantibodies to desmosomal components, desmoglein 1 and 3. Among immunosuppressant therapies, rituximab (RTX) is considered a highly effective treatment with a favorable safety profile, but it induces a prolonged B-cell depletion that can lead to higher susceptibility to infections. For this reason, concerns about its use during the pandemic have been raised. We describe a case of a pemphigus patient in which RTX-induced B cell depletion led to the severe inflammatory phase, whereas corticosteroid treatment allowed a favorable outcome.

In recent years, developing potent antioxidants has been a very active area of research. In this context, phenolic compounds have been evaluated for their antioxidant activity. However, the use of phenolic compounds has also been limited by poor antioxidant activity in several in vivo studies. Polymeric phenols have received much attention owing to their potent antioxidant properties and increased stability in aqueous systems. To be truly effective in biological applications, it is important that these polymers be synthesized using benign methods. In this context, enzyme catalyzed synthesis of polymeric phenols has been explored as an environmentally friendly and safer approach. This review summarizes work in enzymatic syntheses of polymers of phenols. Several assays have been developed to determine the antioxidant potency of these polymeric phenols. These assays are discussed in detail along with structure-property relationships. A deeper understanding of factors affecting antioxidant activity would provide an opportunity for the design of versatile, high performing polymers with enhanced antioxidant activity.

Linear IgA bullous dermatosis (LABD) is characterized by presence of multiple IgA autoantibodies, and a comparatively lesser number of IgG antibodies, directed against different hemidesmosomal antigens. The main autoantigens are LAD-1, LABD-97, BP180 and BP230, type VII collagen and laminin 332. We retrospectively studied the serology of 54 Italian patients with LABD using enzyme-linked immunosorbent assay (ELISA), immunoblotting assay, and indirect immunofluorescence on monkey oesophagus and salt-split skin. Among these, indirect immunofluorescence of salt-split skin elicits the greatest sensitivity. Sixty-three percent of the sera were observed to be positive, with a lamina lucida pattern observed in 48%, a sub-lamina densa pattern in 2% and a mixed pattern in 13% of the cases. IgA reactivity to LAD-1 on immunoblotting was found in 52% of sera, to BP180-NC16A by ELISA in 32% and to BP230 in 26%. Only 17% of patients possessed circulating IgG autoantibodies. LAD-1 was determined to be a major autoantigen of the lamina lucida subtype. Combined serological assays demonstrated a high sensitivity (82%), suggesting that this approach could support diagnosis when a biopsy is not feasible or direct immunofluorescence results are negative.

Journal of the European Academy of Dermatology and VenereologyVolume 34, Issue 3 p. e146-e148 Letter to the Editor Development of bullous pemphigoid in junctional epidermolysis bullosa L. Fania, Corresponding Author L. Fania l.fania@idi.it orcid.org/0000-0003-4194-932X First Dermatologic Division, IDI-IRCCS, Rome, ItalyCorrespondence: L. Fania. E-mail: l.fania@idi.itSearch for more papers by this authorA. Provini, A. Provini First Dermatologic Division, IDI-IRCCS, Rome, ItalySearch for more papers by this authorA. Salemme, A. Salemme Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, ItalySearch for more papers by this authorJ.L. Sinagra, J.L. Sinagra Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, ItalySearch for more papers by this authorL. Guerra, L. Guerra Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, ItalySearch for more papers by this authorC. Mazzanti, C. Mazzanti First Dermatologic Division, IDI-IRCCS, Rome, ItalySearch for more papers by this authorB. Didona, B. Didona First Dermatologic Division, IDI-IRCCS, Rome, ItalySearch for more papers by this authorD. Castiglia, D. Castiglia Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, ItalySearch for more papers by this authorG. Di Zenzo, G. Di Zenzo Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, ItalySearch for more papers by this author L. Fania, Corresponding Author L. Fania l.fania@idi.it orcid.org/0000-0003-4194-932X First Dermatologic Division, IDI-IRCCS, Rome, ItalyCorrespondence: L. Fania. E-mail: l.fania@idi.itSearch for more papers by this authorA. Provini, A. Provini First Dermatologic Division, IDI-IRCCS, Rome, ItalySearch for more papers by this authorA. Salemme, A. Salemme Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, ItalySearch for more papers by this authorJ.L. Sinagra, J.L. Sinagra Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, ItalySearch for more papers by this authorL. Guerra, L. Guerra Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, ItalySearch for more papers by this authorC. Mazzanti, C. Mazzanti First Dermatologic Division, IDI-IRCCS, Rome, ItalySearch for more papers by this authorB. Didona, B. Didona First Dermatologic Division, IDI-IRCCS, Rome, ItalySearch for more papers by this authorD. Castiglia, D. Castiglia Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, ItalySearch for more papers by this authorG. Di Zenzo, G. Di Zenzo Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, ItalySearch for more papers by this author First published: 11 November 2019 https://doi.org/10.1111/jdv.16057Citations: 2Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume34, Issue3March 2020Pages e146-e148 RelatedInformation

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.

Pemphigus vulgaris (PV) is an autoimmune intraepithelial bullous disease. Associations with the class II human leukocyte antigen (HLA) alleles and pemphigus vulgaris have been described. Furthermore, an association between the single nucleotide polymorphism of the ST18 gene and pemphigus vulgaris has been reported. We report two pairs of siblings from two unrelated Italian families affected by pemphigus vulgaris, characterizing their genetic and immunological profile. In order to assess the genetic background, HLA-DQA1, HLA-DQB1, HLA-DRB1 and a relevant ST18 polymorphism were investigated. As for the immunological profiles, anti-desmoglein antibodies were analyzed. In family A, the two pemphigus vulgaris patients had the same HLA genetic profile: HLA-DQA1 *01:04/*03:01, HLA-DQB1 *03:02/*05:03 and HLA-DRB1 *04:02/*14:01. The male patient was heterozygous for the ST18 mutation while the female patient had a wild genotype. In family B, the two pemphigus vulgaris patients were both wild type for the ST18 mutation and showed the same HLA genotype: HLA-DQA1 *03:01/*05:08, HLA-DQB1 *03:01/*03:03 and HLA-DRB1 *04:02/*11:01. Our data show a relevant relationship between the HLA profile and pemphigus vulgaris in our Italian families. In family A, all six alleles are frequently associated with pemphigus vulgaris and were expressed only in the two pemphigus patients; and in family B, two of the six alleles are frequently associated with pemphigus vulgaris. No relevant relationship was found between ST18 polymorphism and pemphigus disease.

The Journal of DermatologyVolume 47, Issue 5 p. e198-e199 Letter to the Editor Serration pattern analysis as a tool for the diagnosis of immunoglobulin A-mediated epidermolysis bullosa acquisita Stefano Senatore, Corresponding Author stef.senatore@gmail.com orcid.org/0000-0001-5891-9587 Section of Dermatology, Department of Health Sciences, University of Florence, Florence, ItalyThese authors contributed equally to this study and should be considered co-first authors. Correspondence: Stefano Senatore, M.D., Section of Dermatology, Department of Health Sciences, University of Florence, Viale Michelangiolo, 41, Florence 50125, Italy. Email: stef.senatore@gmail.comSearch for more papers by this authorRoberto Maglie, orcid.org/0000-0002-5106-4042 Section of Dermatology, Department of Health Sciences, University of Florence, Florence, ItalyThese authors contributed equally to this study and should be considered co-first authors.Search for more papers by this authorAdele Salemme, Molecular and Cell Biology Laboratory, IDI-IRCCS, Rome, ItalySearch for more papers by this authorMarzia Caproni, Section of Dermatology, Department of Health Sciences, University of Florence, Florence, ItalySearch for more papers by this authorGiovanni Di Zenzo, Molecular and Cell Biology Laboratory, IDI-IRCCS, Rome, ItalySearch for more papers by this authorEmiliano Antiga, Section of Dermatology, Department of Health Sciences, University of Florence, Florence, ItalySearch for more papers by this author Stefano Senatore, Corresponding Author stef.senatore@gmail.com orcid.org/0000-0001-5891-9587 Section of Dermatology, Department of Health Sciences, University of Florence, Florence, ItalyThese authors contributed equally to this study and should be considered co-first authors. Correspondence: Stefano Senatore, M.D., Section of Dermatology, Department of Health Sciences, University of Florence, Viale Michelangiolo, 41, Florence 50125, Italy. Email: stef.senatore@gmail.comSearch for more papers by this authorRoberto Maglie, orcid.org/0000-0002-5106-4042 Section of Dermatology, Department of Health Sciences, University of Florence, Florence, ItalyThese authors contributed equally to this study and should be considered co-first authors.Search for more papers by this authorAdele Salemme, Molecular and Cell Biology Laboratory, IDI-IRCCS, Rome, ItalySearch for more papers by this authorMarzia Caproni, Section of Dermatology, Department of Health Sciences, University of Florence, Florence, ItalySearch for more papers by this authorGiovanni Di Zenzo, Molecular and Cell Biology Laboratory, IDI-IRCCS, Rome, ItalySearch for more papers by this authorEmiliano Antiga, Section of Dermatology, Department of Health Sciences, University of Florence, Florence, ItalySearch for more papers by this author First published: 03 March 2020 https://doi.org/10.1111/1346-8138.15161Citations: 2 Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume47, Issue5May 2020Pages e198-e199 RelatedInformation