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Iinterferon-Driven Cutaneous Inflammation in Rosacea and Paradoxical Psoriasis

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Iinterferon-Driven Cutaneous Inflammation in Rosacea and Paradoxical Psoriasis Unicentre CH-1015 Lausanne http://serval.unil.ch RRRRYear : 2017 SIMILAR, YET DISTINCT, PATHOGENIC PATHWAYS OF PLASMACYTOID DENDRITIC CELL-DERIVED TYPE- IINTERFERON-DRIVEN CUTANEOUS INFLAMMATION IN ROSACEA AND PARADOXICAL PSORIASIS Mylonas Alessio Mylonas Alessio, 2017, SIMILAR, YET DISTINCT, PATHOGENIC PATHWAYS OF PLASMACYTOID DENDRITIC CELL-DERIVED TYPE-IINTERFERON-DRIVEN CUTANEOUS INFLAMMATION IN ROSACEA AND PARADOXICAL PSORIASIS Originally published at : Thesis, University of Lausanne Posted at the University of Lausanne Open Archive http://serval.unil.ch Document URN : urn:nbn:ch:serval-BIB_1639D1EEC7550 Droits d’auteur L'Université de Lausanne attire expressément l'attention des utilisateurs sur le fait que tous les documents publiés dans l'Archive SERVAL sont protégés par le droit d'auteur, conformément à la loi fédérale sur le droit d'auteur et les droits voisins (LDA). A ce titre, il est indispensable d'obtenir le consentement préalable de l'auteur et/ou de l’éditeur avant toute utilisation d'une oeuvre ou d'une partie d'une oeuvre ne relevant pas d'une utilisation à des fins personnelles au sens de la LDA (art. 19, al. 1 lettre a). A défaut, tout contrevenant s'expose aux sanctions prévues par cette loi. Nous déclinons toute responsabilité en la matière. Copyright The University of Lausanne expressly draws the attention of users to the fact that all documents published in the SERVAL Archive are protected by copyright in accordance with federal law on copyright and similar rights (LDA). Accordingly it is indispensable to obtain prior consent from the author and/or publisher before any use of a work or part of a work for purposes other than personal use within the meaning of LDA (art. 19, para. 1 letter a). Failure to do so will expose offenders to the sanctions laid down by this law. We accept no liability in this respect. Faculty of Medicine, Department of Dermatology SIMILAR, YET DISTINCT, PATHOGENIC PATHWAYS OF PLASMACYTOID DENDRITIC CELL-DERIVED TYPE-I INTERFERON-DRIVEN CUTANEOUS INFLAMMATION IN ROSACEA AND PARADOXICAL PSORIASIS Doctoral Thesis in Life Sciences (PhD) presented to the Faculty of Biology and Medicine of the University of Lausanne by Alessio Mylonas Master of Science, University of Leicester, United Kingdom Bachelor of Science, University of Sussex, United Kingdom Jury Prof. Daniel Speiser, President Prof. Curdin Conrad, Thesis Director Prof. Julien Seneschal, Expert Prof. Benjamin Marsland, expert Lausanne 2017 Dedicated to my dear parents Also, to everyone who wonders if I’m dedicating this to them. Yes. I am. Acknowledgements It is important for me to thank my mentor, Curdin. Your positive attitude and cheerfulness have motivated me to continue our endeavours well beyond the projects we initially set out to do. As I sat through Prof. Griffiths’ lecture on leadership, I distinctly remember thinking how well you fit the description of a true leader. Equitable, flexible, optimistic. Truly, one in a million. Michel, for inspiring us with your work ethic and good heart. Our own light shines brightest through others’. All my current colleagues, Jeremy, Ana, Alessia, Anna, Sofia, Anissa, and Dorys. And past colleagues Olivier, Nicolas, and Sophie. You were the reason why there was always positive attitude in the lab. Our good friends and collaborators, without whom we wouldn’t have the encouragement to always aspire to do better. In Düsseldorf, Heike Hawerkamp, Dr. Meller, and Professor Homey. In Paris, Yichen Wang and Professor Hovnanian. In Geneva, Luisa and Nicolò. And in gastroenterology Dominique Velin. The Centre for Immunity and Infection Lausanne (CIIL), a satisfying environment suited for pleasant and open research. In the true spirit of Lausanne. Scientific societies for support, in particular the French DC society (CFCD), the Swiss Society for Allergology and Immunology (SSAI), the European Society for Dermatological Research (ESDR). Galderma Spirig for my first award for research, a truly motivating push. All patients that, despite personal discomfort, agree to participate in scientific studies. Science wouldn’t be possible without your courage, so thank you. TABLE OF CONTENTS 1. INTRODUCTION ................................................................................................................................ 11 1.1. THE INNATE AND ADAPTIVE IMMUNE SYSTEM IN THE SKIN ......................................................... 11 1.1.1. THE SKIN, MORE THAN JUST BARRIER................................................................................... 11 1.1.2. INNATE IMMUNITY AGAINST EXOGENOUS INSULTS ................................................................ 13 1.1.3. SKIN ADAPTIVE IMMUNITY IN RESPONSE TO FOREIGN INVASION ............................................. 17 1.2. PATHOGENESIS AND TREATMENT OF PSORIASIS ......................................................................... 19 1.2.1. THE ROLE OF T-CELLS AND TH17/22 CYTOKINES IN DRIVING DISEASE ..................................... 19 1.2.1.1. EVIDENCE FOR RECOGNITION OF SKIN-ASSOCIATED T-CELL ANTIGENS ................................ 19 1.2.1.2. TNF GOVERNS THE INFLAMMATORY MILIEU IN PSORIASIS ................................................. 20 1.2.1.3. PSORIASIS IS MEDIATED BY T-CELL DERIVED TH17 CYTOKINES ............................................ 22 1.2.1.4. MOUNTING A TH17 RESPONSE IN THE SKIN ....................................................................... 23 1.2.2. TYPE-I INTERFERONS AND PLASMACYTOID DENDRITIC CELLS INITIATE PSORIASIS ..................... 24 1.2.3. ANTI-TNFS AND RECENT ADVANCES IN BIOLOGIC THERAPY ................................................... 25 1.3. ANTI-TNF INDUCED PARADOXICAL PSORIASIS ........................................................................... 28 1.3.1. CLINICAL, EPIDEMIOLOGICAL AND HISTOLOGICAL CONSIDERATIONS ........................................ 28 1.3.2. PUTATIVE GENETIC PREDISPOSITION ..................................................................................... 30 1.3.3. MOLECULAR PATHWAYS INDUCED BY TNF BLOCKADE ............................................................ 30 1.4. ROSACEA AND INNATE INFLAMMATION ..................................................................................... 31 1.4.1. CLINICAL, EPIDEMIOLOGICAL AND HISTOLOGICAL CONSIDERATIONS ........................................ 32 1.4.2. ROSACEA MANAGEMENT AND AVAILABLE TREATMENTS ......................................................... 33 1.4.3. ANTI-MICROBIAL PEPTIDES AND EMERGING THERAPIES .......................................................... 33 2. AIMS OF THE STUDY ......................................................................................................................... 37 3. RESULTS .......................................................................................................................................... 39 4. DISCUSSION AND PERSPECTIVES ........................................................................................................ 51 4.1. TYPE-I INTERFERON AT THE CROSSROADS OF PATHOGENIC INNATE AND ADAPTIVE IMMUNITY ......... 51 4.2. UNDESIRED EFFECTS OF TYPE-I INTERFERON BLOCKADE AND OF CYTOKINE IMBALANCE .................... 53 4.3. TYPE-I INTERFERON PRODUCTION BY PDCS AS A DRUGGABLE TARGET ............................................ 54 4.4. UPSTREAM PATHOGENIC TRIGGERS OF TYPE-I INTERFERONS IN SKIN DISEASE ................................. 59 4.5. DOWNSTREAM INNATE MEDIATORS OF TYPE-I INTERFERON-DRIVEN SKIN INFLAMMATION .............. 56 5. APPENDICES .................................................................................................................................... 59 6. BIBLIOGRAPHY ............................................................................................................................... 149 ABSTRACT Cutaneous immunity coordinates necessary protection of the host against exogenous insults, yet its deregulation can have profound pathogenic consequences which can lead to development of disease. Type-I interferons are a class of pro-inflammatory cytokines with fundamental roles in innate and adaptive immune responses. In the skin, they not only mount responses against pathogens and tumours, but also sustain re-epithelialisation following injury, and provide tonic signals for maintaining homeostatic balance. Importantly, they are also involved in the pathogenesis of a number of organ- specific and systemic auto-immune diseases such as systemic lupus, type-I diabetes, and thyroid disease, and in the skin they are important drivers of psoriasis and discoid lupus. Exactly how perturbations of type-I interferons lead to cutaneous disease is still a hotly debated subject of research. Production of type-I interferons, in particular IFNβ, is achieved by all nucleated cells, yet small relative numbers of professional producers exist in the circulation and lymphoid organs, which produce many fold higher amounts of these inflammatory cytokines. Plasmacytoid dendritic cells (pDCs), though generally dispensable for many immune responses, are implicated in several type-I interferon-driven auto-immune diseases. Psoriasis, a TH1/TH17 disease with an important role for Tumour Necrosis Factor (TNF), is just such a disease. Intriguingly, treatment of psoriasis (or other diseases) with a class of biologics called anti- TNFs is effective in most patients, but can also result in the development of novel psoriasiform lesions in about 2-5% of all treated individuals. This side-effect of anti-TNFs,
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