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Autoimmunity in autoinflammatory disease

Gabriela Barcenas-Morales, Peter Jandus, Rainer Döffinger
PURPOSE OF REVIEW: Concise overview of the field of anticytokine autoantibodies with a focus on recent developments. RECENT FINDINGS: Advances in particular in the analysis of autoantibodies to IFNγ, granulocyte-macrophage colony-stimulating factor (GM-CSF) and IFN-1 are presented. The target epitope for anti-IFNγ autoantibodies has been found to have high homology to a protein from Aspergillus suggesting molecular mimicry as a mechanism of breaking self-tolerance...
October 13, 2016: Current Opinion in Allergy and Clinical Immunology
Hagit Peleg, Eldad Ben-Chetrit
PURPOSE OF REVIEW: This article addresses the prevalence and relationship between autoinflammatory diseases and vasculitis. RECENT FINDINGS: Autoimmune diseases (AIDs) are a group of syndromes characterized by episodes of unprovoked inflammation due to dysregulation of the innate immune system. Despite the common occurrence of rashes and other skin lesions in these diseases, vasculitis is reported in only a few. On the other hand, neutrophilic dermatoses are more prevalent...
October 13, 2016: Current Opinion in Rheumatology
Paul Hasler, Stavros Giaglis, Sinuhe Hahn
Polymorphonuclear neutrophil granulocytes are the first responders of the immune system to threats by invading microorganisms. In the traditional view, they combat the intruders by phagocytosis and externalisation of granules containing lytic and microbicidal factors. A dozen years ago, this concept was expanded by the observation that neutrophils may react to bacteria by extruding their nuclear chromosomal DNA with attached nuclear and cytoplasmic constituents to form extracellular reticular structures. Since they trapped and immobilised the microbes, they were designated neutrophil extracellular traps (NETs), and their ensuing cell death NETosis...
2016: Swiss Medical Weekly
Daniel Peckham, Thomas Scambler, Sinisa Savic, Michael F McDermott
Immune-mediated autoinflammatory diseases are occupying an increasingly prominent position among the pantheon of debilitating conditions that afflict mankind. This review focuses on some of the key developments which have occurred since the original description of autoinflammatory disease in 1999, and focuses on underlying mechanisms that trigger autoinflammation. The monogenic autoinflammatory disease range has expanded considerably during that time, and now includes a broad spectrum of disorders, including relatively common conditions such as cystic fibrosis and subsets of systemic lupus erythematosus...
September 29, 2016: Journal of Pathology
Hanna Kim, Gina A Montealegre Sanchez, Raphaela Goldbach-Mansky
Autoinflammatory disorders are sterile inflammatory conditions characterized by episodes of early-onset fever and disease-specific patterns of organ inflammation. Recently, the discoveries of monogenic disorders with strong type I interferon (IFN) signatures caused by mutations in proteasome degradation and cytoplasmic RNA and DNA sensing pathways suggest a pathogenic role of IFNs in causing autoinflammatory phenotypes. The IFN response gene signature (IGS) has been associated with systemic lupus erythematosus (SLE) and other autoimmune diseases...
October 2016: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
Shelly Pathak, Michael F McDermott, Sinisa Savic
The spectrum of systemic autoinflammatory disorders broadens continually. In part, this is due to the more widespread application of massive parallel sequencing, helping with novel gene discovery in this and other areas of rare diseases. Some of the conditions that have been described fit neatly into a conventional idea of autoinflammation. Others, such as interferon-mediated autoinflammatory diseases, are broadening the concept which we consider to be autoinflammatory disorders. There is also a widening of the clinical phenotypes associated with certain genetic mutations, as genetic testing is used more regularly and increasing numbers of patients are screened...
September 19, 2016: Journal of Clinical Pathology
Zhenyu Zhong, Elsa Sanchez-Lopez, Michael Karin
Loss of homeostasis, as a result of pathogen invasion or self imbalance, causes tissue damage and inflammation. In addition to its well-established role in promoting clearance of pathogens or cell corpses, inflammation is also key to drive tissue repair and regeneration. Conserved from flies to humans, a transient, well-balanced inflammatory response is critical for restoration of tissue homeostasis after damage. The absence of such a response can result in failure of tissue repair, leading to the development of devastating immunopathologies and degenerative diseases...
July 2016: Clinical and Experimental Rheumatology
Štefan Blazina, Gašper Markelj, Anja Koren Jeverica, Nataša Toplak, Nevenka Bratanič, Janez Jazbec, Peter Kopač, Maruša Debeljak, Alojz Ihan, Tadej Avčin
An abnormal regulation of immune responses leads to autoimmune and inflammatory manifestations in patients with primary immunodeficiencies (PIDs). The objective of our study was to evaluate the frequency of non-infectious and non-malignant manifestations in a large cohort of patients included in the Slovenian national PID registry and to assess the time of manifestation onset with respect to the time of PID diagnosis. Medical records of registered patients were reviewed. Data on autoimmunity, lymphoproliferation, autoinflammation, allergies, PID diagnosis, and underlying genetic defects were collected and analyzed...
August 31, 2016: Journal of Clinical Immunology
Laura Duffy, Steven C O'Reilly
Autoinflammatory diseases are defined as the loss of self-tolerance in which an inflammatory response to self-antigens occurs, which are a significant global burden. Toll-like receptors are key pattern recognition receptors, which integrate signals leading to the activation of transcription factors and ultimately proinflammatory cytokines. Recently, it has become apparent that these are at the nexus of autoinflammatory diseases making them viable and attractive drug targets. The aim of this review was to evaluate the role of innate immunity in autoinflammatory conditions alongside the role of negative regulation while suggesting possible therapeutic targets...
2016: ImmunoTargets and Therapy
Eoin F McKinney, Kenneth G C Smith
During acute viral infection CD8 T cells rapidly expand before contracting down to a persistent memory population that confers long-lasting immunity. However when the antigen persists, such as during chronic viral infection, a dysfunctional process termed 'exhaustion' limits the antiviral response, facilitating ongoing viraemia and poor clinical outcome. CD8 T cell exhaustion was originally identified in lymphocytic choriomeningitis virus (LCMV) infection of mice however new evidence has shown that exhaustion is associated with the control of a wide range of human chronic inflammatory states including chronic viral infection, autoimmunity and cancer...
August 31, 2016: Immunology and Cell Biology
Gustavo Guimarães Moreira Balbi, Ricardo Azêdo Montes, Verônica Silva Vilela, Marcella Azevedo Borges Andrade, Monisa Martins Nóbrega, Luna Azulay-Abulafia, Roberto Souto da Silva, Evandro Mendes Klumb, Roger Abramino Levy
The term autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA) or Shoenfeld's syndrome refers to a wide group of immune-mediated diseases triggered by external agents. Several substances, such as vaccine adjuvants, squalene and silicone implants, are implied in the pathogenesis of ASIA syndrome. Treatment and prognosis of this complex condition are not completely known due to lack of good quality evidence. After a brief introductory literature review on ASIA, we report here two cases of patients that developed rapidly progressive systemic sclerosis clinical features after multiple intramuscular local injections of a substance recommended by a non-medical professional called ADE...
August 11, 2016: Immunologic Research
Eugen Feist, Gerd-Rüdiger Burmester, Elke Krüger
The ubiquitin proteasome system is closely connected to apoptosis, autophagy, signaling of inflammatory cytokines and generation of ligands for MHC class I antigen presentation. Proteasome function in the innate immune response becomes particularly evident in patients with proteasome-associated autoinflammatory syndromes (PRAAS), where disease causing mutations result in reduced proteasome activity. PRAAS can be classified as a novel type of interferonopathy, however the molecular mechanism and signaling pathways leading from impaired proteasome capacity, the accumulation of damaged proteins, and the induction of type I IFN-genes remain to be determined...
July 27, 2016: Clinical Immunology: the Official Journal of the Clinical Immunology Society
Paola Rizzo, Dario Pitocco, Francesco Zaccardi, Enrico Di Stasio, Rocky Strollo, Alessandro Rizzi, Giuseppe Scavone, Federica Costantini, Marco Galli, Giovanni Tinelli, Andrea Flex, Salvatore Caputo, Paolo Pozzilli, Raffaele Landolfi, Giovanni Ghirlanda, Ahuva Nissim
AIMS: Charcot neuroarthropathy (CN) is a disabling complication, culminating in bone destruction and involving joints and articular cartilage with high inflammatory environment. Its real pathogenesis is as yet unknown. In autoinflammatory diseases, such as rheumatoid arthritis, characterized by inflammation and joint involvement, autoantibodies against oxidative post-translationally modified (oxPTM) collagen type I (CI) and type II (CII) were detected. Therefore, the aim of our study was to assess the potential involvement of autoimmunity in charcot neuroarthropathy, investigating the presence of autoantibodies oxPTM-CI and oxPTM-CII, in participants with charcot neuroarthropathy...
July 25, 2016: Diabetes/metabolism Research and Reviews
Pawel Majewski, Monika Majchrzak-Gorecka, Beata Grygier, Joanna Skrzeczynska-Moncznik, Oktawia Osiecka, Joanna Cichy
Neutrophil extracellular traps (NETs), DNA webs released into the extracellular environment by activated neutrophils, are thought to play a key role in the entrapment and eradication of microbes. However, NETs are highly cytotoxic and a likely source of autoantigens, suggesting that NET release is tightly regulated. NET formation involves the activity of neutrophil elastase (NE), which cleaves histones, leading to chromatin decondensation. We and others have recently demonstrated that inhibitors of NE, such as secretory leukocyte protease inhibitor (SLPI) and SerpinB1, restrict NET production in vitro and in vivo...
2016: Frontiers in Immunology
Marije I Koenders, Wim B van den Berg
Rheumatic disease is not a single disorder, but a group of more than 100 diseases that affect joints, connective tissues, and/or internal organs. Although rheumatic diseases like rheumatoid arthritis (RA), psoriatic arthritis, and ankylosing spondylitis (AS) differ in their pathogenesis and clinical presentation, the treatment of these inflammatory disorders overlaps. Non-steroid anti-inflammatory drugs are used to reduce pain and inflammation. Additional disease-modifying anti-rheumatic drugs are prescribed to slowdown disease progression, and is in RA more frequently and effectively applied than in AS...
2016: Drug Design, Development and Therapy
Arianne C Richard, James E Peters, James C Lee, Golnaz Vahedi, Alejandro A Schäffer, Richard M Siegel, Paul A Lyons, Kenneth G C Smith
BACKGROUND: Tumour necrosis factor (TNF) superfamily cytokines and their receptors regulate diverse immune system functions through a common set of signalling pathways. Genetic variants in and expression of individual TNF superfamily cytokines, receptors and signalling proteins have been associated with autoimmune and inflammatory diseases, but their interconnected biology has been largely unexplored. METHODS: We took a hypothesis-driven approach using available genome-wide datasets to identify genetic variants regulating gene expression in the TNF superfamily cytokine signalling network and the association of these variants with autoimmune and autoinflammatory disease...
2016: Genome Medicine
Sujani Yadlapati, Petros Efthimiou
Specific autoimmune and inflammatory rheumatic diseases have been associated with an increased risk of malignant lymphomas. Conditions such as rheumatoid arthritis (RA), primary Sjögren's syndrome (pSS), systemic lupus erythematosus (SLE), dermatomyositis, and celiac disease have been consistently linked to malignant lymphomas. Isolated cases of lymphomas associated with spondyloarthropathies and autoinflammatory diseases have also been reported. Direct association between autoimmunity and lymphomagenesis has been reinforced by large epidemiological studies...
2016: BioMed Research International
Nina Chevalier, Jian K Tan, Linda J Mason, Remy Robert, Craig I McKenzie, Florence Lim, Connie H Wong, Laurence Macia, Alison N Thorburn, Brendan E Russ, Seth L Masters, Charles R Mackay
Environmental factors contribute to development of autoimmune diseases. For instance, human autoimmune arthritis can associate with intestinal inflammation, cigarette smoking, periodontal disease, and various infections. The cellular and, molecular pathways whereby such remote challenges might precipitate arthritis or flares remain unclear. Here, we used a transfer model of self-reactive arthritis-inducing CD4(+) cells from KRNtg mice that, upon transfer, induce a very mild form of autoinflammatory arthritis in recipient animals...
September 2016: Journal of Autoimmunity
Giuseppe Patuzzo, Alessandro Barbieri, Elisa Tinazzi, Dino Veneri, Giuseppe Argentino, Francesca Moretta, Antonio Puccetti, Claudio Lunardi
Common variable immunodeficiency (CVID) is a heterogeneous group of diseases, characterized by primary hypogammaglobulinemia. B and T cell abnormalities have been described in CVID. Typical clinical features of CVID are recurrent airway infections; lymphoproliferative, autoinflammatory, or neoplastic disorders; and autoimmune diseases among which autoimmune thrombocytopenia (ITP) is the most common. The coexistence of immunodeficiency and autoimmunity appears paradoxical, since one represents a hypoimmune state and the other a hyperimmune state...
September 2016: Autoimmunity Reviews
Frieda A Koopman, Sangeeta S Chavan, Sanda Miljko, Simeon Grazio, Sekib Sokolovic, P Richard Schuurman, Ashesh D Mehta, Yaakov A Levine, Michael Faltys, Ralph Zitnik, Kevin J Tracey, Paul P Tak
Rheumatoid arthritis (RA) is a heterogeneous, prevalent, chronic autoimmune disease characterized by painful swollen joints and significant disabilities. Symptomatic relief can be achieved in up to 50% of patients using biological agents that inhibit tumor necrosis factor (TNF) or other mechanisms of action, but there are no universally effective therapies. Recent advances in basic and preclinical science reveal that reflex neural circuits inhibit the production of cytokines and inflammation in animal models...
July 19, 2016: Proceedings of the National Academy of Sciences of the United States of America
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