Lupus erythematosus-like imiquimod reaction: a diagnostic pitfall*

Barr, Keira; Konia, Thomas; Fung, Maxwell A.

doi:10.1111/j.1600-0560.2010.01592.x

Cited by 14 publications

(28 citation statements)

References 33 publications

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“…4 Natural ligands of TLR7 in DM patients probably include microbial RNA since a clinical history consistent with an infection is frequently reported prior to disease onset, 7 but endogenous RNAs are also likely to be involved notably during cancer and UV radiation damages, two frequent local conditions involving TLR7-mediated response 8 9 and triggering DM. Consistently with this view, skin TLR7 activation in mice 10 and human 11 has been previously reported to trigger lupus, an autoimmune disease that is also characterised by a type on interferon signature in blood. These data indicate that TLR7 may represent a therapeutic target in DM.…”

Section: Key Messagessupporting

confidence: 64%

Dermatomyositis flare on imiquimod therapy highlights a crucial role of aberrant TLR7 signalling

et al. 2016

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Section: Key Messagessupporting

confidence: 64%

Dermatomyositis flare on imiquimod therapy highlights a crucial role of aberrant TLR7 signalling

et al. 2016

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“…Similar to psoriasis, cutaneous lesions of lupus are frequently associated with PDC infiltrates (). Furthermore, topical application of imiquimod led to a histopathologic pattern similar to that of cutaneous lupus in humans (). Thus, it is likely that the pathogenesis of both psoriasis and lupus share roles of PDCs and type I IFN.…”

Section: Discussionmentioning

confidence: 99%

Epicutaneous Application of Toll‐like Receptor 7 Agonists Leads to Systemic Autoimmunity in Wild‐Type Mice: A New Model of Systemic Lupus Erythematosus

Yokogawa

Takaishi

Nakajima

et al. 2014

Arthritis & Rheumatology

203

220

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Objective. To examine whether topical treatment of wild-type mice with Toll-like receptor 7 (TLR-7) agonists leads to lupus-like autoimmunity.Methods. Wild-type FVB/N, BALB/c, and C57BL/6 mice were treated with the topical TLR-7 agonist imiquimod or R848 administered to the ear 3 times weekly. During treatment, the mice were monitored for serum autoantibody and creatinine levels as well as histopathology of the kidneys, spleens, livers, hearts, and skin. Immunologic abnormalities were analyzed by immunohistochemistry, quantitative reverse transcription-polymerase chain reaction, and fluorescence-activated cell sorting. The role of plasmacytoid dendritic cells (PDCs) in the development of autoimmune disease was validated by in vivo treatment with an anti-PDC antibody. Diseased mice underwent ultraviolet B irradiation, to evaluate skin photosensitivity. The disease-causing effect of topical application of imiquimod was compared with that of systemic (intraperitoneal) administration. TLR-7-and TLR-9-deficient mice were used to validate the role of TLR-7.Results. Wild-type mice of different genetic backgrounds developed systemic autoimmune disease following 4 weeks of topical treatment with imiquimod or R848, with elevated levels of autoantibodies to doublestranded DNA and multiple organ involvement, including glomerulonephritis, hepatitis, carditis, and photosensitivity. Expression of Ifna and Mx1, the interferon-␣-stimulated gene, was up-regulated in the organs of imiquimod-treated mice. However, disease caused by intraperitoneal injection of imiquimod was less severe than that induced by topical application. In vivo depletion of PDCs by a specific antibody protected mice against the autoimmunity induced by topical administration of imiquimod, suggesting a role of PDCs. Furthermore, TLR-7-deficient mice, but not TLR-9-deficient mice, were protected against autoimmunity.Conclusion. This protocol provides a novel model of inducible systemic lupus erythematosus in wild-type mice and underscores the skin as the primary organ that allows TLR-7 agonists to induce SLE.

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“…Moreover, 0.5% R‐salbutamol cream, a β2‐adrenergic receptor agonist, showed promising results in a double‐blind, randomized controlled phase II trial, but has never been approved for CLE and is – to our knowledge – not commercially available as topical agent . Imiquimod is a topical immune response‐modifying drug with controversial results in CLE lesions …”

Section: Methodsmentioning

confidence: 99%

“…45 Imiquimod is a topical immune response-modifying drug with controversial results in CLE lesions. [46][47][48][49][50][51]…”

Section: Recommendationsmentioning

confidence: 99%

S2k guideline for treatment of cutaneous lupus erythematosus – guided by the European Dermatology Forum (EDF) in cooperation with the European Academy of Dermatology and Venereology (EADV)

Kuhn

Aberer

Bata‐Csörgő

et al. 2016

Acad Dermatol Venereol

147

182

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Cutaneous lupus erythematosus (CLE) is a rare inflammatory autoimmune disease with heterogeneous clinical manifestations. To date, no therapeutic agents have been licensed specifically for patients with this disease entity, and topical and systemic drugs are mostly used 'off-label'. The aim of the present guideline was to achieve a broad consensus on treatment strategies for patients with CLE by a European subcommittee, guided by the European Dermatology Forum (EDF) and supported by the European Academy of Dermatology and Venereology (EADV). In total, 16 European participants were included in this project and agreed on all recommendations. Topical corticosteroids remain the mainstay of treatment for localized CLE, and further topical agents, such as calcineurin inhibitors, are listed as alternative first-line or second-line topical therapeutic option. Antimalarials are recommended as first-line and long-term systemic treatment in all CLE patients with severe and/or widespread skin lesions, particularly in patients with a high risk of scarring and/or the development of systemic disease. In addition to antimalarials, systemic corticosteroids are recommended as first-line treatment in highly active and/or severe CLE. Second-and third-line systemic treatments include methotrexate, retinoids, dapsone and mycophenolate mofetil or mycophenolate acid, respectively. Thalidomide should only be used in selected therapy-refractory CLE patients, preferably in addition to antimalarials. Several new therapeutic options, such as B-cell-or interferon a-targeted agents, need to be further evaluated in clinical trials to assess their efficacy and safety in the treatment of patients with CLE. JEADVAll authors are participants of the European Society for Cutaneous Lupus Erythematosus (EUSCLE), which received a grant by the European Academy of Dermatology and Venereology (EADV) to perform the project. This grant was used to organize the consensus conferences and to reimburse the travel fees and the accommodation of each participant. In addition, the grant by the EADV was used to partly reimburse the personnel costs of Aysche Landmann for coordination of the project; and drafting, copy-editing and formatting of the manuscript. Elisabeth Aberer, Zsuszanna Bata-Cs€ org€ o, Marcia Caproni, Andreas Dreher, Camille Frances, Regine Gl€ aser, Hans-Wilhelm Kl€ otgen, Annegret Kuhn, Aysche Landmann, Branka Marinovic, Filippa Nyberg, Rodica Olteanu, Annamari Ranki and Beatrix Volc-Platzer have no conflicts of interest with regard to fees for participation in review activities, such as data monitoring boards, statistical analysis, or end point committees. Jacek C. Szepietowski participated in the Novartis Steering Committee and the Sandoz Data Monitoring Committee. Elisabeth Aberer, Zsuszanna Bata-Cs€ org€ o, Marcia Caproni, Andreas Dreher, Camille Frances, Regine Gl€ aser, Hans-Wilhelm Kl€ otgen, Annegret Kuhn, Branka Marinovic, Filippa Nyberg, Rodica Olteanu, Annamari Ranki, Jacek C. Szepietowski and Beatrix Volc-Platzer have no confl...

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Lupus erythematosus-like imiquimod reaction: a diagnostic pitfall*

Cited by 14 publications

References 33 publications

Dermatomyositis flare on imiquimod therapy highlights a crucial role of aberrant TLR7 signalling

Dermatomyositis flare on imiquimod therapy highlights a crucial role of aberrant TLR7 signalling

Epicutaneous Application of Toll‐like Receptor 7 Agonists Leads to Systemic Autoimmunity in Wild‐Type Mice: A New Model of Systemic Lupus Erythematosus

S2k guideline for treatment of cutaneous lupus erythematosus – guided by the European Dermatology Forum (EDF) in cooperation with the European Academy of Dermatology and Venereology (EADV)

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