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      Mogamulizumab-Associated Cutaneous Granulomatous Drug Eruption Mimicking Mycosis Fungoides but Possibly Indicating Durable Clinical Response

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          Abstract

          This case series report of mogamulizumab-associated cutaneous granulomatous drug eruption (CGDE) describes 12 patients with mycosis fungoides (MF) whose CGDE mimicked the MF but was followed by durable clinical MF response.

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          Mogamulizumab versus vorinostat in previously treated cutaneous T-cell lymphoma (MAVORIC): an international, open-label, randomised, controlled phase 3 trial

          Javier Munoz, Amy Musiek, Andrei Shustov … (2018)
          Cutaneous T-cell lymphomas are rare non-Hodgkin lymphomas with substantial morbidity and mortality in advanced disease stages. We compared the efficacy of mogamulizumab, a novel monoclonal antibody directed against C-C chemokine receptor 4, with vorinostat in patients with previously treated cutaneous T-cell lymphoma.
          Article 0 comments Cited 186 times – based on 0 reviews     Review now
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            Macrophage Epithelial Reprogramming Underlies Mycobacterial Granuloma Formation and Promotes Infection.

            Mark Cronan, Rebecca W. Beerman, Allison Rosenberg … (2016)
            Mycobacterium tuberculosis infection in humans triggers formation of granulomas, which are tightly organized immune cell aggregates that are the central structure of tuberculosis. Infected and uninfected macrophages interdigitate, assuming an altered, flattened appearance. Although pathologists have described these changes for over a century, the molecular and cellular programs underlying this transition are unclear. Here, using the zebrafish-Mycobacterium marinum model, we found that mycobacterial granuloma formation is accompanied by macrophage induction of canonical epithelial molecules and structures. We identified fundamental macrophage reprogramming events that parallel E-cadherin-dependent mesenchymal-epithelial transitions. Macrophage-specific disruption of E-cadherin function resulted in disordered granuloma formation, enhanced immune cell access, decreased bacterial burden, and increased host survival, suggesting that the granuloma can also serve a bacteria-protective role. Granuloma macrophages in humans with tuberculosis were similarly transformed. Thus, during mycobacterial infection, granuloma macrophages are broadly reprogrammed by epithelial modules, and this reprogramming alters the trajectory of infection and the associated immune response.
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              Sarcoidosis--scientific progress and clinical challenges.

              D Moller, Shun-Hua Chen (2011)
              Sarcoidosis is an uncommon systemic inflammatory disorder characterized by noncaseating granulomatous inflammation that most commonly affects the lungs, intrathoracic lymph nodes, eyes and skin. One-third or more of patients with sarcoidosis have chronic, unremitting inflammation with progressive organ impairment. Findings of family and genetic studies indicate a genetic susceptibility to sarcoidosis, with genes in the MHC region having a dominant role. Immunologic hallmarks of the disease include highly polarized expression of cytokines produced by type 1 T helper cells and tumor necrosis factor (TNF) at sites of inflammation. Increasing evidence obtained within the past decade suggests the etiology of sarcoidosis predominantly involves microbial triggers, with the most convincing data implicating mycobacterial or propionibacterial organisms. Innate immune mechanisms, possibly involving misfolding and aggregation of serum amyloid A, might have a critical role in the pathobiology of sarcoidosis. Despite these advances, there are no clinically useful biomarkers that can assist the clinician in diagnosis, prognosis or assessment of treatment effects. Corticosteroids remain the cornerstone of therapy when organ function is threatened or progressively impaired. The role of immunosuppressive drugs and anti-TNF agents in the treatment of sarcoidosis remains uncertain, and there are no FDA-approved therapies. Meaningful progress in developing clinically useful tools and new therapies will depend on further advances in understanding the pathogenesis of sarcoidosis and its disease-specific pathways.
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                Author and article information

                Journal
                Title: JAMA Dermatology
                Abbreviated Title: JAMA Dermatol
                Publisher: American Medical Association (AMA)
                ISSN (Print): 2168-6068
                Publication date Created: August 01 2019
                Publication date (Print): August 01 2019
                Volume: 155
                Issue: 8
                Page: 968
                Affiliations
                [1 ]Division of Dermatology, Department of Medicine, Washington University School of Medicine in St Louis, St Louis, Missouri
                [2 ]The Ronald O. Perelman Department of Dermatology, New York University School of Medicine, New York
                [3 ]Division of Medical Oncology, Department of Medicine, Washington University School of Medicine in St Louis, St Louis, Missouri
                [4 ]St Louis Veterans Health Administration Medical Center, St Louis, Missouri
                [5 ]Flatiron Health Inc, New York, New York
                [6 ]Department of Pathology and Immunology, Washington University School of Medicine in St Louis, St Louis, Missouri
                [7 ]Tallahassee Associates of Dermatology, Florida State University College of Medicine, Tallahassee, Florida
                Article
                DOI: 10.1001/jamadermatol.2019.0369
                PMC ID: 6547069
                PubMed ID: 31141114
                SO-VID: de572f30-cac8-4e9b-a39c-0a52ed9e3480
                Copyright © © 2019
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