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In this review, we will dissect the microbial actors thought to be involved in the HH as well as their immunomodulatory mechanisms as emphasized by experimental studies, with a particular attention on parasites. Thereafter, we will review the early clinical trials using helminthes’ derivatives focusing on autoimmune diseases. 
BrainImmune's comment,
May 5, 2015 4:46 AM
you are welcome Alfredo
Alfredo Corell's comment,
May 5, 2015 6:03 PM
:)
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The prevalence of thyroid autoimmunity in patients with #urticaria: a systematic review and meta-analysis. http://t.co/RLgLl7jRna
Alfredo Corell's insight:
ENDOCRINE, July 27th, 2014 The meta-analysis results showed that the prevalence of positive thyroid autoantibodies in patients with urticaria was higher than non-urticaria controls (TgAb: OR 6.55, 95 % CI 3.19–13.42, P < 0.00001, I 2 = 67 %; TmAb: OR 4.51, 95 % CI 2.78–7.33, P < 0.00001, I 2 = 47 %; TPOAb: OR 8.71, 95 % CI 6.89–11.01,P < 0.00001, I 2 = 20 %, respectively). The results of this meta-analysis suggested that patients with urticaria were more likely to have thyroid autoimmunity than the control groups.
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I first came across the term “celiac disease autoimmunity” a few weeks ago as I read summaries of the article “Risk of Pediatric Celiac Disease According to HLA Haplotype and Country” that was published in the July 3, 2014 issue of the New England Journal of Medicine (NEJM).
Alfredo Corell's insight:
Liu E, Lee HS, Aronsson CA, et al. TEDDY Study Group. Risk of pediatric celiac disease according to HLA haplotype and country. N Engl J Med. 2014 Jul 3;371(1):42-9.
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Special Issues in Autoimmunity Reviews and Journal of Autoimmunity
Alfredo Corell's insight:
Special Issues in Autoimmunity Reviews and Journal of Autoimmunity Autoimmunity Reviews and the Journal of Autoimmunity both feature a special issue on diagnostic criteria in autoimmune diseases, to coincide with the 9th International Congress on Autoimmunity in Nice, France, in March 2014. Here you can read both issues – free access until June 2014. Diagnostic Criteria in Autoimmune Diseases Diagnostic Criteria in Autoimmune Diseases
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Those in self-nonself camp, the more dominant of the two camps, would see a threat in the molecular mimics and link those to autoimmunity. Whereas the danger or damage theory proponents would argue that the presence or absence of molecular mimicry by itself means nothing unless the mimicked code evokes damage. Data can be found supporting either argument.
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A Cure for Chlamydia Arthritis?
Alfredo Corell's insight:
Abstract
Chlamydia trachomatis and Chlamydia pneumoniae together comprise the most frequent causative pathogens that elicit reactive arthritis (ReA). Advances in our understanding of the molecular biology/molecular genetics of these organisms have improved significantly the ability to detect chlamydiae in the joint for diagnostic purposes, as well as extending our current understanding of the pathogenic processes they elicit in the joint and elsewhere. An important aspect of the latter is that synovial chlamydiae infect the joint in an unusual but metabolically active state. While some standard treatments can provide a palliative effect on the ReA disease phenotype, many reports have indicated that standard antibiotic treatment does not provide a cure. Of critical importance, however, two recent reports of controlled clinical trials demonstrated that Chlamydia-ReA can be treated successfully using combination antibiotic therapy. These observations offer the opportunity of a cure for this disease, thereby increasing the practical importance of awareness and diagnosis of the spondyloarthritis caused by Chlamydia. In this viewpoint, we provide an overview of recent key findings in the epidemiology, pathophysiology, clinical manifestations, diagnosis and treatment of Chlamydia-induced arthritis. Our intention is for these insights to be translated rapidly into clinical practice to overcome misdiagnosis and underdiagnosis of the disease, and for them to stimulate the continued development of a cure. Primary source: Annals of the Rheumatic Diseases
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Press release about a research to be presented in the American Academy of Neurology 66th Annual Meeting. Better be cautious and patient with this information: in the study only 16 patients vs 16 healthy controls have been studied. A too small cohort to make a strong conclusion.
Alfredo Corell's insight:
PHILADELPHIA – An antibody found in the blood of people with multiple sclerosis (MS) may be present long before the onset of the disease and its symptoms, according to a study released today that will be presented at theAmerican Academy of Neurology’s 66th Annual Meeting in Philadelphia, April 26 to May 3, 2014.
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fascinating review of costimulatory pathway drugs in inflammation & autoimmunity... did bench work on many of these! http://t.co/sPaZK8nR9d
Alfredo Corell's insight:
Targeting co-stimulatory pathways: transplantation and autoimmunity
Nature Reviews Nephrology 10, 14-24 (2014) doi:10.1038/nrneph.2013.183 Ultimately, understanding the interplay between individual co-stimulatory and co-inhibitory pathways engaged during T-cell activation and
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A major challenge in human genetics is to devise a systematic strategy to integrate disease-associated variants with diverse genomic and biological data sets to provide insight into disease pathogenesis and guide drug discovery for complex traits...
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Liver Disease Diagnostics: Antibody-Based Diagnosis of Autoimmune Liver Disease For the launch of our Liver-9-Line immunoblot test (to our press release “Liver Disease Diagnostics by Immunoblot” of May 16, 2011), I dug through a pile of literature...
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Here we report that proliferation of Treg cells after TCR stimulation is impaired in subjects with relapsing-remitting multiple sclerosis (RRMS) because of altered interleukin-2 (IL-2) secretion and IL-2 receptor (IL-2R)-signal ... Via Krishan Maggon
Alfredo Corell's insight:
Original article: http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.3411.html NATURE MEDICINE | LETTER Regulatory T cell proliferative potential is impaired in human autoimmune diseaseFortunata Carbone,Veronica De Rosa,Pietro B Carrieri,Silvana Montella,Dario Bruzzese,Antonio Porcellini,Claudio Procaccini,Antonio La Cava& Giuseppe Matarese
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Alfredo Corell's insight:
November 6, 2013Autoantibodies Present Before Symptom Onset in Primary Sjögren SyndromeRoland Jonsson, DMD, PhD1; Elke Theander, MD, PhD2; Bitte Sjöström, MSc3; Karl Brokstad, PhD1; Gunnel Henriksson, MD, PhD3[+] Author AffiliationsJAMA. 2013;310(17):1854-1855. doi:10.1001/jama.2013.278448.
The news in Medical Press: http://medicalxpress.com/news/2013-11-autoantibodies-blood-years-symptom-onset.html
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Monogenic autoinflammatory diseases are a group of hereditary disorders characterized by a clinical and biological inflammatory syndrome in which there is little or no evidence of autoimmunity.
Alfredo Corell's insight:
Dowonload the complete "provisional" pdf: http://www.ojrd.com/content/pdf/1750-1172-8-162.pdf ;
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Abstract:
Autoimmune encephalitis (AIE) associated with neural autoantibodies is increasingly recognized as a cause of subacute onset amnesia, confusion, and seizures. In the past decade, several key antibody targets have been identified in AIE. These include the N-methyl D-aspartate (NMDA) receptors, voltage-gated potassium channel complexes—in particular leucine-rich glioma inactivated 1 (LGI1) and glutamic acid decarboxylase (GAD). There is accumulating clinical and laboratory evidence that antibodies targeting the extracellular domains of cell-surface molecules are directly pathogenic. Each antibody target associates with a spectrum of clinical features and relative response to immunotherapies. These immunotherapies have been shown to improve short- and long-term clinical outcomes in affected patients. AIE is an important differential diagnosis to consider in patients presenting with symptoms of encephalitis as early diagnosis can lead to successful treatment. 2013 Citation European Neurological Review, 2014;9(1):87–92 Correspondence: Sarosh R Irani, DPhil, MRCP (Neurol), Level 6, West Wing, John Radcliffe Hospital, Oxford, OX3 9DS, UK. E: sarosh.irani@ndcn.ox.ac.uk
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Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK ...
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Small fiber neuropathy, rather than central sensitization, may be responsible for the pain associated with fibromyalgia, some researchers have hypothesized. (Autoimmunity anyone ? If if walks and talks and smells like it .....
Alfredo Corell's insight:
Primary source: Arthritis & Rheumatology
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Highlights
Alfredo Corell's insight:
Abstract
Sjögren's syndrome (SS) is an autoimmune disease characterized primarily by lymphocytic infiltration of the exocrine glands, and autoantibody production. Multiple environmental factors affecting an individual with a genetic susceptibility may trigger the development of SS. Herein, we aimed to evaluate links between the different pebbles in the mosaic of SS. Demographic, clinical data and blood samples were gathered from 82 consecutive patients with SS, and 139 healthy controls. Samples were analyzed for infectious serology and auto-antibodies as well as for relevant genetic mutations (TAP genes) and cytokines levels. An immune response (IgG) against Epstein–Barr virus (EBV) early antigen (EA) was positively associated with SS (OR 4; 95% CI: 1.82–8.83, p = 0.001) while a protective effect of IgG anti-cytomegalovirus (CMV) was observed (OR 0.3; 95%CI: 0.16–0.74, p = 0.009). Anti-Ro/SSA, anti-LA/SSB, anti-nuclear, anti-gliadin, anti-TTG-IgG and anti-RNP antibodies were statistically more prevalent among SS patients than controls. Notably, the presence of anti-Ro/SSA and anti La/SSB correlated with anti-EBVEA IgG (OR 3.1; 95%CI: 1.08–8.74) and (OR 3.9; 95%CI: 1.37–10.96) respectively. Autoantibodies, cytokines and several genetic markers correlated with clinical manifestation of SS. Our data suggest that infectious agents may play both a causative and protective role in the pathogenesis of SS. Moreover certain autoantibodies, cytokines and specific TAP alleles correlate with clinical manifestations of SS, and may enable better prediction and/or directed therapy once confirmed in future studies.
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En la historia de la lucha contra el sida, tener una enfermedad adicional a la infección por el VIH a veces depara sorpresas. Lo hizo en el caso de Timothy Brown, el famoso pacient
Alfredo Corell's insight:
Videoentrevista al autor del articulo: Artículo en el Journal of Clinical Investigation:
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Largest Microbiome Study on Newly Diagnosed Patients Gives Insight Into Crohn's Disease and Shows Antibiotic Treatment May Worsen Disease
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Summary
Inflammatory bowel diseases (IBDs), including Crohn’s disease (CD), are genetically linked to host pathways that implicate an underlying role for aberrant immune responses to intestinal microbiota. However, patterns of gut microbiome dysbiosis in IBD patients are inconsistent among published studies. Using samples from multiple gastrointestinal locations collected prior to treatment in new-onset cases, we studied the microbiome in the largest pediatric CD cohort to date. An axis defined by an increased abundance in bacteria which include Enterobacteriaceae, Pasteurellacaea, Veillonellaceae, and Fusobacteriaceae, and decreased abundance in Erysipelotrichales, Bacteroidales, and Clostridiales, correlates strongly with disease status. Microbiome comparison between CD patients with and without antibiotic exposure indicates that antibiotic use amplifies the microbial dysbiosis associated with CD. Comparing the microbial signatures between the ileum, the rectum, and fecal samples indicates that at this early stage of disease, assessing the rectal mucosal-associated microbiome offers unique potential for convenient and early diagnosis of CD. Divulgative news: http://www.sys-con.com/node/3009818
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Daily Mail Study: Culprit leading to rheumatoid arthritis discovered Asahi Shimbun “We can expect to develop a drug that is targeted at denatured proteins to dissolve them, or a method of examination that will allow doctors to make a diagnosis of...
Alfredo Corell's insight:
Significance Cellular misfolded proteins are transported to the cell surface by MHC class II molecules via association with the peptide-binding groove without processing to peptides. We found that IgG heavy chain is transported to the cell surface by MHC class II molecules. Furthermore, IgG heavy chain associated with MHC class II molecules is recognized by autoantibodies in rheumatoid arthritis patients. Autoantibody binding to IgG heavy chain complexed with different MHC class II alleles was strongly associated with rheumatoid arthritis susceptibility conferred by certain MHC class II alleles. These findings suggest that misfolded proteins complexed with MHC class II molecules could be targets for autoantibodies in autoimmune diseases, which might be involved in autoimmune disease susceptibility. Link to PNAS publication: http://www.pnas.org/content/early/2014/02/19/1401105111.short
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Vitamin A used in acne medicines may help autoimmune and transplant patients Science Codex "The results will help us to use the different protocol of Treg induction for clinical therapy in autoimmune diseases and organ transplantation protection,'"...
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The original research article is published in The Journal of Leukocyte Biology:
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Tregitope applications may include any of the autoimmune diseases that are currently treated almost exclusively with intravenous immunoglobulin G (IVIG), such as Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) and Multifocal Motor Neuropathy (MMN), as well as gene therapy and allergy where Tregitopes may provide a means of inducing antigen-specific tolerance.
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Link to the journal: http://www.hindawi.com/journals/jir/2013/493138/ Download pdf: http://downloads.hindawi.com/journals/cdi/2013/493138.pdf
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Autoimmunity Reviews
Volume 12, Issue 11, September 2013, Pages 1076–1084 Benedetta Marigliano, Alessandra Soriano, Domenico Margiotta, Marta Vadacca, Antonella AfeltraAbstract The lungs are frequently involved in Connective Tissue Diseases (CTDs). Interstitial lung disease (ILD) is one of the most common pleuropulmonary manifestations that affects prognosis significantly. In practice, rheumatologists and other physicians tend to underestimate the impact of CTD-ILDs and diagnose respiratory impairment when it has reached an irreversible fibrotic stage. Early investigation, through clinical evidence, imaging and – in certain cases – lung biopsy, is therefore warranted in order to detect a possible ILD at a reversible initial inflammatory stage. In this review, we focus on lung injury during CTDs, with particular attention to ILDs, and examine their prevalence, clinical manifestations and histological patterns, as well as therapeutic approaches and known complications till date. Although several therapeutic agents have been approved, the best treatment is still not certain and additional trials are required, which demand more knowledge of pulmonary involvement in CTDs. Our central aim is therefore to document the impact that lung damage has on CTDs. We will mainly focus on Rheumatoid Arthritis (RA), which – unlike other rheumatic disorders – resembles Idiopathic Pulmonary Fibrosis (IPF) in numerous aspects.
Gilbert C FAURE's curator insight,
December 15, 2013 11:32 AM
rheumatoid lung is histologicaly frequent according to some autopsy studies but seldomly clinically diagnosed already 4 pages of scoops related to rheumatoid arthritis http://www.scoop.it/t/rheumatology-rhumatologie?q=rheumatoid+art
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New study that identifies a possible causative link between gut microbiota and sex hormone production that may drive protection from autoimmunity.
Alfredo Corell's insight:
Science. 2013 Mar 1;339(6123):1084-8. doi: 10.1126/science.1233521. Epub 2013 Jan 17.Sex differences in the gut microbiome drive hormone-dependent regulation of autoimmunity.Markle JG, Frank DN, Mortin-Toth S, Robertson CE, Feazel LM, Rolle-Kampczyk U, von Bergen M, McCoy KD, Macpherson AJ, Danska JS.Source
Program in Genetics and Genome Biology, Hospital for Sick Children Research Institute, Toronto, Ontario, Canada. AbstractMicrobial exposures and sex hormones exert potent effects on autoimmune diseases, many of which are more prevalent in women. We demonstrate that early-life microbial exposures determine sex hormone levels and modify progression to autoimmunity in the nonobese diabetic (NOD) mouse model of type 1 diabetes (T1D). Colonization by commensal microbes elevated serum testosterone and protected NOD males from T1D. Transfer of gut microbiota from adult males to immature females altered the recipient's microbiota, resulting in elevated testosterone and metabolomic changes, reduced islet inflammation and autoantibody production, and robust T1D protection. These effects were dependent on androgen receptor activity. Thus, the commensal microbial community alters sex hormone levels and regulates autoimmune disease fate in individuals with high genetic risk.
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Alfredo Corell's insight:
“Too much” adaptive immune activity leads to autoimmunity. “Too much” innate immune activity leads to autoinflammation. Autoimmune diseases are abnormalities of the adaptive immune system, autoinflammatory diseases are abnormalities of innate immunity.
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Background
The Hygiene Hypothesis (HH) attributes the dramatic increase in autoimmune and allergic diseases observed in recent decades in Western countries to the reduced exposure to diverse immunoregulatory infectious agents. This theory has since largely been supported by strong epidemiological and experimental evidence.
BMC Medicine 2015, 13:81 doi:10.1186/s12916-015-0306-7
The electronic version of this article is the complete one and can be found online at:http://www.biomedcentral.com/1741-7015/13/81