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Autoimmunity in autoinflammatory disease

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https://www.readbyqxmd.com/read/29038114/inflammasome-dependent-cytokines-at-the-crossroads-of-health-and-autoinflammatory-disease
#1
Hanne Van Gorp, Nina Van Opdenbosch, Mohamed Lamkanfi
As key regulators of both innate and adaptive immunity, it is unsurprising that the activity of interleukin (IL)-1 cytokine family members is tightly controlled by decoy receptors, antagonists, and a variety of other mechanisms. Additionally, inflammasome-mediated proteolytic maturation is a prominent and distinguishing feature of two important members of this cytokine family, IL-1β and IL-18, because their full-length gene products are biologically inert. Although vital in antimicrobial host defense, deregulated inflammasome signaling is linked with a growing number of autoimmune and autoinflammatory diseases...
October 16, 2017: Cold Spring Harbor Perspectives in Biology
https://www.readbyqxmd.com/read/28950818/inflammation-and-epilepsy-preclinical-findings-and-potential-clinical-translation
#2
Gaetano Terrone, Alessia Salamone, Annamaria Vezzani
BACKGROUND: The lack of treatments which can prevent epilepsy development or improve disease prognosis represents an unmet and urgent clinical need. The development of such drugs requires a deep understanding of the mechanisms underlying disease pathogenesis. In the last decade, preclinical studies in models of acute seizures and of chronic epilepsy highlighted that neuroinflammation arising in brain areas of seizure onset and generalization is a key contributor to neuronal hyper-excitability underlying seizure generation...
September 25, 2017: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28934246/discovery-of-pf-06928215-as-a-high-affinity-inhibitor-of-cgas-enabled-by-a-novel-fluorescence-polarization-assay
#3
Justin Hall, Amy Brault, Fabien Vincent, Shawn Weng, Hong Wang, Darren Dumlao, Ann Aulabaugh, Dikran Aivazian, Dana Castro, Ming Chen, Jeffrey Culp, Ken Dower, Joseph Gardner, Steven Hawrylik, Douglas Golenbock, David Hepworth, Mark Horn, Lyn Jones, Peter Jones, Eicke Latz, Jing Li, Lih-Ling Lin, Wen Lin, David Lin, Frank Lovering, Nootaree Niljanskul, Ryan Nistler, Betsy Pierce, Olga Plotnikova, Daniel Schmitt, Suman Shanker, James Smith, William Snyder, Timothy Subashi, John Trujillo, Edyta Tyminski, Guoxing Wang, Jimson Wong, Bruce Lefker, Leslie Dakin, Karen Leach
Cyclic GMP-AMP synthase (cGAS) initiates the innate immune system in response to cytosolic dsDNA. After binding and activation from dsDNA, cGAS uses ATP and GTP to synthesize 2', 3' -cGAMP (cGAMP), a cyclic dinucleotide second messenger with mixed 2'-5' and 3'-5' phosphodiester bonds. Inappropriate stimulation of cGAS has been implicated in autoimmune disease such as systemic lupus erythematosus, thus inhibition of cGAS may be of therapeutic benefit in some diseases; however, the size and polarity of the cGAS active site makes it a challenging target for the development of conventional substrate-competitive inhibitors...
2017: PloS One
https://www.readbyqxmd.com/read/28928270/the-evolving-role-of-the-rheumatologist-in-the-management-of-immune-related-adverse-events-iraes-caused-by-cancer-immunotherapy
#4
EDITORIAL
Leonard Calabrese, Xavier Mariette
The rapid introduction of immunotherapies for cancer-targeting immunological checkpoints has led to a new class of toxicities that appear to be of autoimmune and or autoinflammatory origin. These disorders are now referred to as immune-related adverse events (irAEs) and pose considerable challenges to patient care in terms of how to optimally manage these formidable toxicities while allowing effective antitumoural therapy to continue. While rheumatologists will naturally be called on to manage those irAEs of rheumatic origin, we believe there is a need and an opportunity for rheumatologists to participate as central figures in this evolving field, in large part because of our familiarity with multiorgan autoimmune disease and our expertise in crafting and utilising both traditional and biological immune-based therapies...
September 19, 2017: Annals of the Rheumatic Diseases
https://www.readbyqxmd.com/read/28918934/reconstructive-microsurgical-approach-for-the-treatment-of-pyoderma-gangrenosum
#5
Karl Schwaiger, Elisabeth Russe, Hassan Kholosy, Michaela Hladik, Klemens Heinrich, Laurenz Weitgasser, Thomas Schoeller, Gottfried Wechselberger
INTRODUCTION: Pyoderma gangrenosum (PG) is a rare type of autoimmune disease that results in progressive ulcers with or without previous trauma. However, PG is not well understood to date, and its treatment therefore remains a challenge. Because of the disease's systemic characteristic and the unpredictability of the clinical course, no gold standard treatment is available, especially concerning the surgical procedures to treat pyodermic lesions. Often, PG is not recognized during routine clinical practice, and standard ulcer treatment (conservative wound care, debridement, skin grafting, and local flap coverage) is initiated; this induces an autoinflammatory response, resulting in disastrous ulcers, thereby making free flap coverage necessary...
August 16, 2017: Journal of Plastic, Reconstructive & Aesthetic Surgery: JPRAS
https://www.readbyqxmd.com/read/28900629/siae-rare-variants-in-juvenile-idiopathic-arthritis-and-primary-antibody-deficiencies
#6
Eirini Sevdali, Elena Tsitsami, Maria Tsinti, Evangelia Farmaki, Efimia Papadopoulou-Alataki, Anastasios E Germenis, Matthaios Speletas
Sialic acid acetylesterase (SIAE) deficiency was suggested to lower the levels of ligands for sialic acid-binding immunoglobulin-like receptors, decreasing the threshold for B-cell activation. In humans, studies of rare heterozygous loss-of-function mutations in SIAE gene in common autoimmune diseases, including juvenile idiopathic arthritis (JIA), yielded inconsistent results. Considering the distinct pathogenesis of the two main subtypes of JIA, autoinflammatory systemic (sJIA) and autoimmune oligo/polyarticular (aJIA), and a predisposition to autoimmunity displayed by patients and families with primary antibody deficiencies (PADs), the aim of our study was to analyze whether SIAE rare variants are associated with both the phenotype of JIA and the autoimmunity risk in families with PADs...
2017: Journal of Immunology Research
https://www.readbyqxmd.com/read/28888842/evidence-refuting-the-existence-of-autoimmune-autoinflammatory-syndrome-induced%C3%A2-by-adjuvants-asia
#7
Rohan Ameratunga, David Gillis, Michael Gold, Allan Linneberg, J Mark Elwood
Autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA) was described in 2011. Over time the condition and its triggers have broadened to include several autoimmune disorders, the macrophagic myofasciitis syndrome, the Gulf war syndrome, the sick building syndrome, siliconosis, and the chronic fatigue syndrome. The aluminum-containing adjuvants in the hepatitis B vaccine and the human papillomavirus vaccine in particular have been stated to be the major causes of the disorder. Here, we review the specificity of the diagnostic criteria for ASIA...
September 6, 2017: Journal of Allergy and Clinical Immunology in Practice
https://www.readbyqxmd.com/read/28866302/hemophagocytic-syndrome-primary-forms-and-predisposing-conditions
#8
REVIEW
Fernando E Sepulveda, Geneviève de Saint Basile
Hemophagocytic lymphohistiocytosis (HLH, also referred to a hemophagocytic syndrome) is a life-threatening condition in which uncontrolled activation of lymphocytes and macrophages, and thus the secretion of large amounts of inflammatory cytokines, leads to a severe hyperinflammatory state. Over the last few decades, researchers have characterized primary forms of HLH caused by genetic defects that impair lymphocytes' cytotoxic machinery. Other genetic causes of HLH not related to impaired cytotoxicity have also recently been identified...
August 31, 2017: Current Opinion in Immunology
https://www.readbyqxmd.com/read/28830446/autoimmune-phenotype-with-type-i-interferon-signature-in-two-brothers-with-ada2-deficiency-carrying-a-novel-cecr1-mutation
#9
Andrea Skrabl-Baumgartner, Barbara Plecko, Wolfgang M Schmidt, Nadja König, Michael Hershfield, Ursula Gruber-Sedlmayr, Min Ae Lee-Kirsch
BACKGROUND: Loss-of-function CECR1 mutations cause polyarteritis nodosa (PAN) with childhood onset, an autoinflammatory disorder without significant signs of autoimmunity. Herein we describe the unusual presentation of an autoimmune phenotype with constitutive type I interferon activation in siblings with adenosine deaminase 2 (ADA2) deficiency. CASE PRESENTATION: We describe two siblings with early-onset recurrent strokes, arthritis, oral ulcers, discoid rash, peripheral vascular occlusive disease and high antinuclear antibody titers...
August 22, 2017: Pediatric Rheumatology Online Journal
https://www.readbyqxmd.com/read/28808967/purification-of-cyclic-gmp-amp-from-viruses-and-measurement-of-its-activity-in-cell-culture
#10
Alice Mayer, Jonathan Maelfait, Anne Bridgeman, Jan Rehwinkel
Sensing of cytoplasmic DNA by cGAS is essential for the initiation of immune responses against several viruses. cGAS also plays important roles in some autoinflammatory and autoimmune diseases and may be involved in immune responses targeting cancer cells. Once activated, cGAS catalyzes the formation of the di-nucleotide 2'-3'-cyclic GMP-AMP (cGAMP), which propagates a signaling cascade leading to the production of type I interferons (IFNs). Interestingly, cGAMP is incorporated into enveloped viruses and is transferred to newly infected cells by virions...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28806468/an-overview-of-hemophagocytic-lymphohistiocytosis
#11
Ysabella M Esteban, Jill L O de Jong, Melissa S Tesher
Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening syndrome characterized by a dysregulated hyperinflammatory response associated with aberrant activation of lymphocytes and macrophages that results in hypercytokinemia. It is classically divided into two types: (1) primary or familial HLH and (2) secondary HLH. Familial HLH is generally an autosomal recessive condition, whereas secondary HLH is usually associated with infectious diseases, autoinflammatory and autoimmune diseases (where it is more commonly known as macrophage activation syndrome), malignancy, immunosuppression, hematopoietic stem cell transplantation, organ transplantation, HIV infection, and metabolic diseases...
August 1, 2017: Pediatric Annals
https://www.readbyqxmd.com/read/28798075/cytokines-of-the-il-1-family-recognized-targets-in-chronic-inflammation-underrated-in-organ-transplantations
#12
REVIEW
Ilja Striz
Interleukin 1 (IL-1) family is a group of cytokines with multiple local and systemic effects, which regulates both innate and adaptive immune responses. Generally, most IL-1 family cytokines express prevailing pro-inflammatory activities (IL-1α, IL-1β, IL-18, IL-33, IL-36 α, β, γ), whereas others are anti-inflammatory (IL-1Ra (IL-1 receptor antagonist), IL-36Ra, IL-38, IL-37). In addition to their immunomodulatory roles, some of them are also involved in the physiological modulation of homeostatic processes and directly affect mRNA transcription...
September 1, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28790368/signs-of-innate-immune-activation-and-premature-immunosenescence-in-psoriasis-patients
#13
Liisi Šahmatova, Elena Sügis, Marina Šunina, Helen Hermann, Ele Prans, Maire Pihlap, Kristi Abram, Ana Rebane, Hedi Peterson, Pärt Peterson, Külli Kingo, Kai Kisand
Psoriasis is a chronic inflammatory disease that affects skin and is associated with systemic inflammation and many serious comorbidities ranging from metabolic syndrome to cancer. Important discoveries about psoriasis pathogenesis have enabled the development of effective biological treatments blocking the T helper 17 pathway. However, it has not been settled whether psoriasis is a T cell-mediated autoimmune disease or an autoinflammatory disorder that is driven by exaggerated innate immune signalling. Our comparative gene expression and hierarchical cluster analysis reveal important gene circuits involving innate receptors...
August 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28771701/cellular-metabolism-of-tumor-associated-macrophages-functional-impact-and-consequences
#14
REVIEW
Katrin Rabold, Mihai G Netea, Gosse J Adema, Romana T Netea-Maier
Macrophages are innate immune cells that play a role not only in host defense against infections, but also in the pathophysiology of autoimmune and autoinflammatory disorders, as well as cancer. An important feature of macrophages is their high plasticity, with high ability to adapt to environmental changes by adjusting their cellular metabolism and immunological phenotype. Macrophages are one of the most abundant innate immune cells within the tumor microenvironment that have been associated with tumor growth, metastasis, angiogenesis and poor prognosis...
October 2017: FEBS Letters
https://www.readbyqxmd.com/read/28738209/psoriasis-a-mixed-autoimmune-and-autoinflammatory-disease
#15
REVIEW
Yun Liang, Mrinal K Sarkar, Lam C Tsoi, Johann E Gudjonsson
In recent years marked progress has been made in our understanding of the critical biologic and immunologic pathways involved in psoriasis. Genetic studies have demonstrated that susceptibility to psoriasis involves components of both the adaptive and innate immune system and not surprisingly activation of both of these arms of the immune system is found in psoriatic skin. While adaptive immune responses predominate in chronic plaque psoriasis, innate and autoinflammatory responses dominate in pustular forms of psoriasis, with other clinical subtypes extending on a spectrum between plaque and pustular psoriasis...
July 21, 2017: Current Opinion in Immunology
https://www.readbyqxmd.com/read/28733143/mechanisms-of-nlrp1-mediated-autoinflammatory-disease-in-humans-and-mice
#16
REVIEW
Chien-Hsiung Yu, Jonas Moecking, Matthias Geyer, Seth L Masters
NLRP1 was the first NOD-like receptor described to form an inflammasome, recruiting ASC to activate caspase-1, which processes interleukin-1β and interleukin-18 to their active form. A wealth of new genetic information has now redefined our understanding of this innate immune sensor. Specifically, rare loss-of-function variants in the N-terminal pyrin domain indicate that this part of NLRP1 is autoinhibitory and normally acts to prevent a familial autoinflammatory skin disease associated with cancer. In the absence of a ligand to trigger human NLRP1, these mutations have now confirmed the requirement of NLRP1 autolytic cleavage within the FIIND domain, which had previously been implicated in NLRP1 activation...
July 19, 2017: Journal of Molecular Biology
https://www.readbyqxmd.com/read/28724326/sting-signalling-an-emerging-common-pathway-in-autoimmunity-and-cancer
#17
David McCaffary
The equipoise between the disease states of cancer and autoinflammation has perhaps been underappreciated in clinical practice and biomedical research. However, since the discover of STING (stimulator of interferon genes) as an integral regulator of innate immunity, a wealth of information has implicated this signaling pathway in both of these diseases. Under cellular homeostasis, STING serves to detect - and promote immune defense against - DNA viruses and intracellular bacteria, as described in its initial discovery...
July 20, 2017: Immunopharmacology and Immunotoxicology
https://www.readbyqxmd.com/read/28722725/the-monogenic-autoinflammatory-diseases-define-new-pathways-in-human-innate-immunity-and-inflammation
#18
REVIEW
Kalpana Manthiram, Qing Zhou, Ivona Aksentijevich, Daniel L Kastner
Autoinflammatory diseases were first recognized nearly 20 years ago as distinct clinical and immunological entities caused by dysregulation in the innate immune system. Since then, advances in genomic techniques have led to the identification of new monogenic disorders and their corresponding signaling pathways. Here we review these monogenic autoinflammatory diseases, ranging from periodic fever syndromes caused by dysregulated inflammasome-mediated production of the cytokine IL-1β to disorders arising from perturbations in signaling by the transcription factor NF-κB, ubiquitination, cytokine signaling, protein folding, type I interferon production and complement activation, and we further examine their molecular mechanisms...
July 19, 2017: Nature Immunology
https://www.readbyqxmd.com/read/28694138/does-type-i-interferon-drive-systemic-autoimmunity
#19
REVIEW
Cécile Picard, Alexandre Belot
Type-I interferon (IFN)-mediated immune response involves both innate and adaptive immune system and has a pivotal role in antiviral defence. A complex interplay of intracellular signaling pathways and tight regulatory systems drive the IFN activation. The observation of an aberrant stimulation of this system as a common molecular basis in peculiar inherited autoimmune and autoinflammatory disorders led to the concept of "type I interferonopathies". But the precise genetic dissection of this growing spectrum of diseases adds more and more complexity to the comprehension of this concept and a lot of unsolved questions remain such as how type I IFN can drive systemic inflammation in these clinically and genetically heterogeneous diseases...
July 8, 2017: Autoimmunity Reviews
https://www.readbyqxmd.com/read/28690611/insight-into-the-endocrine-system-and-the-immune-system-a-review-of-the-inflammatory-role-of-prolactin-in-rheumatoid-arthritis-and-psoriatic-arthritis
#20
REVIEW
Man W Tang, Samuel Garcia, Danielle M Gerlag, Paul P Tak, Kris A Reedquist
Rheumatoid arthritis (RA) is a chronic autoimmune disease that affects females three times more frequently than males. A potential role for hormones, such as prolactin (PRL), may in part explain this phenomenon. The risk of developing RA is increased in women who are lactating after the first pregnancy, which might be related to breastfeeding and the release of PRL. Other studies found a protective effect of PRL on RA development. Some studies have reported that hyperprolactinemia is more common in RA and serum PRL levels are correlated with several disease parameters, although others could not confirm these findings...
2017: Frontiers in Immunology
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