Read a free sample or buy Antiphospholipid Syndrome by Laurent Phialy, Stéphane Zuily & Doruk Erkan. You can read this book with iBooks on your iPhone, iPad, iPod touch, or Mac.
Gilbert C FAURE's insight:
Our Antiphospholipid Syndrome (APS) iBook presentation at ACR2017 Annual Meeting with Stéphane ZUILY, Jessica R Berman, and Laurent Phialy. "Based on our international two-center randomized control study of medical students, a classroom APS lecture is the most effective method in improving medical students’ knowledge, when compared to self-learning methods, i.e., APS iBook or APS printed material. Among these two self-learning methods, medical students were more satisfied with the APS iBook, although both resulted in the same degree of improvement of knowledge." Thank you @Hospital for Special Surgery Medical Education Academy for supporting this project. You can download APS iBook free @ https://lnkd.in/dm3aJnz
The International Congress on Antiphospholipid Antibodies (aPL) is held every three years to discuss the recent advances and future directions in aPL and Antiphospholipid Syndrome (APS). On behalf of the Local and International Executive Committees, it is my pleasure to invite you to the 15th International Congress on aPL, which will take place in Istanbul, Turkey, on September 21-24, 2016.
Objective: To measure antiphospholipid antibody (aPL) variance during pregnancy; to determine if variation affects outcomes. Methods: We used data from PROMISSE, a multicenter prospective study of pregnant women with aPL and/or SLE.
ObjectivesThe objective of this study was to assess the contribution of clinically significant antiphospholipid antibodies (aPL) to organ damage in systemic lupus erythematosus (SLE).MethodsPatients with disease duration of less than 10 years and...
Anti-phospholipid antibody syndrome (APS) is a systemic autoimmune disease characterized clinically by arterial and/or venous thromboses, recurrent abortions or fetal loss and serologically by the presence of ‘anti-phospholipid...
Gilbert C FAURE's insight:
Anti-phospholipid antibody syndrome (APS) is a systemic autoimmune disease characterized clinically by arterial and/or venous thromboses, recurrent abortions or fetal loss and serologically by the presence of ‘anti-phospholipid antibodies’ (aPL). The main target antigen of the antibodies is β2glycoprotein I (β2GPI). Post-translational oxidative modifications of the protein have been widely described. In this study we aimed to analyse sera reactivity to glucose-modified β2GPI (G-β2GPI). Sera collected from 43 patients with APS [15 primary APS (PAPS) and 28 APS associated with systemic lupus erythematosus (SLE) (SAPS)], 30 with SLE, 30 with rheumatoid arthritis (RA) and 40 healthy subjects were analysed by an enzyme-linked immunosorbent assay (ELISA) using a G-β2GPI. Nine of 15 consecutive PAPS out-patients (60%) and 16 of 28 SAPS (57.1%) showed serum antibodies [immunoglobulin (Ig)G class] against G-β2GPI (anti-G-β2GPI) by ELISA. The occurrence of anti-G-β2GPI was significantly higher in APS patients compared to patients suffering from SLE. No RA patients or control healthy subjects resulted positive for anti-G-β2GPI. Of note, aG-β2GPI prompted to identify some APS patients (four PAPS and seven SAPS), who were negative in the classical anti-β2GPI test. Moreover, in APS patients, anti-G-β2GPI titre was associated significantly with venous thrombosis and seizure in APS patients. This study demonstrates that G-β2GPI is a target antigen of humoral immune response in patients with APS, suggesting that β2GPI glycation products may contain additional epitopes for anti-β2GPI reactivity. Searching for these antibodies may be useful for evaluating the risk of clinical manifestations.
Systemic lupus erythematosus (SLE) has preponderance in women in their childbearing years; consequently pregnancy has always been an important issue of concern for the patient and the treating physician.
The International Congress on Antiphospholipid Antibodies (aPL) is held every three years to discuss the recent advances and future directions in aPL and Antiphospholipid Syndrome (APS). On behalf of the Local and International Executive Committees, it is my pleasure to invite you to the 15th International Congress on aPL, which will take place in Istanbul, Turkey, on September 21-24, 2016.
William L. Nichols, M.D., discusses testing guidelines for lupus anticoagulant and antiphospholipid antibodies as part of the Mayo Medical Laboratories sympo...
"Cambridge life sciences group Abzena and University College London are collaborating to develop a novel autoimmune therapy to tackle a major disorder of the immune system."
All our team is thrilled to invite you to participate in the 10th Meeting of the European Forum on Antiphospholipid Antibodies which will be held in Nancy, France, on April 27-28, 2017.
Of note, a master class in French will be organized by the French Society of Vascular Medicine on April 29, 2017. This Forum meeting will be the best place for the European clinicians and scientists involved in the field of APS to meet and strengthen current or future collaborations. As in previous meetings, there will be no registration fee for the speakers and attendees. However, hotel and travel expenses should be covered by participants. Each participant must complete the registration form. Additionally, we also invite sponsors and people working on APS though they are not members of the Forum, yet.
Nancy together with organizers will provide to the participants the opportunity to experience the historical, cultural and culinary delights of the city. Looking forward to seeing you all in April 2017 in Nancy. Dr. Jessie Risse, Prof. Stéphane Zuily and Prof. Denis Wahl
Gilbert C FAURE's insight:
We will be present, submitting a communication entitled
Knowledge management in Immunology with Content Curation.
Objectives Patients with antiphospholipid syndrome (APS) are at risk for subclinical endothelial injury, as well as accelerated atherosclerosis. In the related disease systemic lupus erythematosus, there is a well-established defect in circulating endothelial progenitors, which leads to an accrual of endothelial damage over time. This defect has been at least partially attributed to exaggerated expression of type I interferons (IFNs). We sought to determine whether these pathways are important in APS. Methods We studied 68 patients with primary APS. Endothelial progenitors were assessed by flow cytometry and functional assay. Type I IFN activity was determined by a well-accepted bioassay, while peripheral blood mononuclear cells were scored for expression of IFN-responsive genes. Results Endothelial progenitors from patients with APS demonstrated a marked defect in the ability to differentiate into endothelial cells, a phenotype which could be mimicked by treating control progenitors with APS sera. Elevated type I IFN activity was detected in the circulation of patients with APS (a finding that was then replicated in an independent cohort). While IgG depletion from APS sera did not rescue endothelial progenitor function, the dysfunction was successfully reversed by a type I IFN receptor-neutralising antibody. Conclusions We describe, for the first time to our knowledge, an IFN signature in primary APS and show that this promotes impaired endothelial progenitor function. This work opens the door to novel approaches that may mitigate vascular damage in APS, such as anti-IFN drugs.
Read a free sample or buy Antiphospholipid Syndrome by Laurent Phialy, Stéphane Zuily & Doruk Erkan. You can read this book with iBooks on your iPhone, iPad, iPod touch, or Mac.
Anti-phospholipid antibody syndrome (APS) is a systemic autoimmune disease characterized clinically by arterial and/or venous thromboses, recurrent abortions or fetal loss and serologically by the presence of ‘anti-phospholipid antibodies’ (aPL).
The International Congress on Antiphospholipid Antibodies (aPL) is held every three years to discuss the recent advances and future directions in aPL and Antiphospholipid Syndrome (APS). On behalf of the Local and International Executive Committees, it is my pleasure to invite you to the 15th International Congress on aPL, which will take place in Istanbul, Turkey, on September 21-24, 2016.
Objective Pregnancies in women with the antiphospholipid syndrome (APS) are frequently complicated by fetal loss and intrauterine growth restriction (IUGR).
Peptides are known to be targets of autoreactive T cells that can cause autoimmune diseases. Here we show that human T cells recognize self-lipids displayed on the surface of cells by CD1b proteins. A particular lipid that is recognized by CD1b autoreactive cells, phosphatidylglycerol, is present in mammalian mitochondria and in bacteria. Therefore, these data define a phospholipid autoantigen that is released during mitochondrial stress and bacterial infection.
Abstract
In contrast with the common detection of T cells that recognize MHC, CD1a, CD1c, or CD1d proteins, CD1b autoreactive T cells have been difficult to isolate in humans. Here we report the development of polyvalent complexes of CD1b proteins and carbohydrate backbones (dextramers) and their use in identifying CD1b autoreactive T cells from human donors. Activation is mediated by αβ T-cell receptors (TCRs) binding to CD1b-phospholipid complexes, which is sufficient to activate autoreactive responses to CD1b-expressing cells. Using mass spectrometry and T-cell responses to scan through the major classes of phospholipids, we identified phosphatidylglycerol (PG) as the immunodominant lipid antigen. T cells did not discriminate the chemical differences that distinguish mammalian PG from bacterial PG. Whereas most models of T-cell recognition emphasize TCR discrimination of differing self and foreign structures, CD1b autoreactive T cells recognize lipids with dual self and foreign origin. PG is rare in the cellular membranes that carry CD1b proteins. However, bacteria and mitochondria are rich in PG, so these data point to a more general mechanism of immune detection of infection- or stress-associated lipids.
lipid antigen CD1b self-antigen T cell dendritic cell
Human autoreactive T cells recognize CD1b and phospholipidsIldiko Van Rhijn, Twan van Berlo, Tamara Hilmenyuk, Tan-Yun Cheng, Benjamin J. Wolf, Raju V. V. Tatituri, Adam P. Uldrich, Giorgio Napolitani, Vincenzo Cerundolo, John D. Altman,Peter Willemsen, Shouxiong Huang, Jamie Rossjohn, Gurdyal S. Besra, Michael B. Brenner,Dale I. Godfrey, and D. Branch Moody
PNAS 2016 113 (2) 380-385; published ahead of print November 30, 2015,doi:10.1073/pnas.1520947112
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