68 research outputs found
HLA-DRB1 the notorious gene in the mosaic of autoimmunity
No full textThe major histocompatibility complex system is the most polymorphic gene cluster of the mammal genome. In humans, this is a genomic locus known as the human leukocyte antigen (HLA) system. The HLA encodes mostly immune-associated proteins whose main effect is the presentation of antigens to the immune cells. Thus, it is clear that it is essential for to the proper function of the immune response against pathogens and strongly implicated in the development of autoimmune diseases. Nonetheless, there are hundreds of polymorphisms of HLA-DRB1 which have been associated with different autoimmune disorders as well as with immune response to infection and vaccines. It is possible that the interaction of specific HLA with pathogenic antigens is one of the keys favoring (or protecting) toward the development of an autoimmune disease. In the era of personalized medicine, it would be of great help to build a map of the genomic risk of each individual to evaluate the risk of developing an autoimmune condition
Retraído: los autoanticuerpos anti-ribosomal-fosfoproteína penetran en las células neuronales a través de la proteína asociada al crecimiento neuronal, afectando las células neuronales in vitro
No full textThe above article from Rheumatology ‘Anti-ribosomal-phosphoprotein autoantibodies penetrate to neuronal cells via neuronal growth associated protein, affecting neuronal cells in vitro’ by Shaye Kivity, Yehuda Shoenfeld, Maria-Teresa Arango, Dolores J. Cahill, Sara Louise O`Kane, Margalit Zusev, Inna Slutsky, Michal Harel-Meir, Joab Chapman, Torsten Matthias and Miri Blank, published online on 06 May 2016 by Oxford University Press, has been retracted by agreement between the journal Editor, Dr Jacob M. van Laar, The British Society for Rheumatology and Oxford University Press. The retraction has been agreed due to the discovery of significant errors relating to methods and presentation of results
Association Between Autoantibodies and Neuropsychiatric Manifestations of Autoimmune Disease: Comment on the Article by Lauvsnes et al
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The 2014 ACR annual meeting: a bird's eye view of autoimmunity in 2015
No full textOur understanding of the mechanisms leading to rheumatic diseases is growing at unprecedented pace thanks to the worldwide network of clinical and translational researchers who gather at major scientific meetings to share their progresses. Further, these meetings allow the contamination of unrelated research areas and thus the spreading of ideas, hypotheses, and research tools. The annual meeting of the American College of Rheumatology (ACR) serves this purpose by allowing thousands of rheumatologists, immunologists, health care professionals, and basic scientists to attend the same sessions and present their work. The 2014 ACR meeting was held in Boston, MA, and was attended by over 16,000 participants who had the opportunity to directly witness the presentation of over 3000 abstracts. As such is the case, a full attendance of all update opportunities was not feasible. To fill this gap we arbitrarily selected the abstracts the appeared most interesting in a few fields of interest and we herein discuss the presented data and their further implications. In particular, we were intrigued by research advances in biomarkers for rheumatic diseases, and by advances on Sjögren syndrome, neuropsychiatric systemic lupus erythematosus, fibromyalgia, and B cell mechanisms. While we are well aware of the numerous blind spots that are expected in this type of article, we submit that this is far from a comprehensive overview and refer to the abstract book for a more complete analysis of the presented abstracts
Is narcolepsy a classical autoimmune disease?
No full textNarcolepsy is a neurological disorder characterized by excessive daytime sleepiness. It is caused by the loss of orexin producing neurons in the lateral hypothalamus. Current evidences suggest an autoimmune mediated process causing the specific loss of orexin neurons. The high association of the disease with the HLA DQB1?06:02, as well as the link with environmental factors and are important clues supporting this theory. Recently, the association between the occurrence of the disease and vaccination campaign after the 2009 H1N1 pandemic highlighted the importance to increase the knowledge in the Pandora box of the vaccines. This review discusses the last finding regarding the pathogenesis of the disease and its relationship with the H1N1 vaccines. © 2014 Elsevier Ltd. All rights reserved
16/6-idiotype expressing antibodies induce brain inflammation and cognitive impairment in mice: the mosaic of central nervous system involvement in lupus
No full textBackground: The 16/6-idiotype (16/6-Id) of the human anti-DNA antibody was found to induce experimental lupus in naive mice, manifested by production of autoantibodies, leukopenia and elevated inflammatory markers, as well as kidney and brain involvement. We assessed behavior and brain pathology of naive mice injected intracerebra-ventricularly (ICV) with the 16/6-Id antibody. \ud
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Methods: C3H female mice were injected ICV to the right hemisphere with the human 16/6-Id antibody or commercial human IgG antibodies (control). The mice were tested for depression by the forced swimming test (FST), locomotor and explorative activity by the staircase test, and cognitive functions were examined by the novel object recognition and Y-maze tests. Brain slices were stained for inflammatory processes. \ud
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Results: 16/6-Id injected mice were cognitively impaired as shown by significant differences in the preference for a new object in the novel object recognition test compared to controls (P = 0.012). Similarly, the preference for spatial novelty in the Y-maze test was significantly higher in the control group compared to the 16/6-Id-injected mice (42% vs. 9%, respectively, P = 0.065). Depression-like behavior and locomotor activity were not significantly different between the16/6-Id-injected and the control mice. Immunohistochemistry analysis revealed an increase in astrocytes and microglial activation in the hippocampus and amygdala, in the 16/6-Id injected group compared to the control. \ud
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Conclusions: Passive transfer of 16/6-Id antibodies directly into mice brain resulted in cognitive impairments and histological evidence for brain inflammation. These findings shed additional light on the diverse mosaic pathophysiology of neuropsychiatric lupus
Biological Therapies in Inflammatory Myopathies
No full textIdiopathic inflammatory myopathies (IIM) are a rare group of disorders that feature progressive immune-mediated skeletal muscle destruction along with skin, lung, and joint involvement. Management of IIMs necessitates glucocorticoid therapy followed by conventional steroid-sparing agents to control disease activity. In the settings of refractory myositis or life-threatening manifestations, e.g. lung involvement or oropharyngeal dysphagia, second-line therapies are needed to minimize disease burden, avoid end-organ damage and steroid toxicity, and decrease mortality. These therapies may include biological disease-modifying antirheumatic drugs (bDMARDs), and to a lesser extent, targeted synthetic disease-modifying antirheumatic drugs (TSD). This article reviews the current use of bDMARDs, e.g. intravenous immunoglobulin and rituximab, and a TSD—Janus kinase inhibitors (JAKI)—along with their indications, efficacy, and safety in managing IIM
Clinical indications for intravenous immunoglobulin utilization in a tertiary medical center: a 9-year retrospective study
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