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Pathology, Diagnosis and Therapies
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Autoimmunity

Pathology, Diagnosis and Therapy

Gilbert C FAURE's insight:

Autoimmunity is indeed one of the biggest challenge of Immunology!

Understanding the mechanisms of this physiological immune phenomenon inducing such a diverse array of diseases, joint and muscular, digestive, endocrinological, neurological, cutaneous..

 

Improving the molecular and cellular tools in use for a few decades for diagnosis and follow-up of patients, perhaps screening in the future

Mastering the molecular and cellular therapies to treat patients.

 

You can also find relevant informations on some other topics curated  here such as

Rheumatology http://www.scoop.it/t/rheumatology-rhumatologie

Immunology and biotherapies http://www.scoop.it/t/immunology-and-biotherapies

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Studies Unable to Reproduce Results of Two Diabetes Papers

Studies Unable to Reproduce Results of Two Diabetes Papers | AUTOIMMUNITY | Scoop.it
The original work found that an anti-malaria drug or the neurotransmitter GABA could increase the number of insulin-producing pancreatic cells in mice.
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Frontiers | The Interplay Between Keratinocytes and Immune Cells in the Pathogenesis of Psoriasis | Immunology

Frontiers | The Interplay Between Keratinocytes and Immune Cells in the Pathogenesis of Psoriasis | Immunology | AUTOIMMUNITY | Scoop.it
Psoriasis is a chronic inflammatory skin disease resulting from genetic, epigenetic, environmental, and lifestyle factors. To date, several immunopathogenic mechanisms of psoriasis have been elucidated, and, in the current model, the crosstalk between autoreactive T cells and resident keratinocytes generates inflammatory and immune circuits responsible for the initiation, progression and persistence of the disease. Several autoantigens derived from keratinocytes (i. e. LL37 cathelecidin/nucleic acid complexes, newly generated lipid antigens) have been identified which may trigger initial activation of T cells, particularly IL-17-producing T cells, T-helper (Th)1 and Th22 cells. Hence, lymphokines released in skin lesions are pivotal for keratinocyte activation and production of inflammatory molecules which in turn lead to amplification of the local immune responses. Intrinsic genetic alterations of keratinocytes in the activation of signal transduction pathways dependent on T-cell derived cytokines are also fundamental. The current review emphasizes the aberrant interplay of immune cells and skin resident keratinocytes in establishing and sustaining inflammatory and immune responses in psoriasis.
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Autoantibodies, detection methods and panels for diagnosis of Sjögren's syndrome - ScienceDirect

Autoantibodies, detection methods and panels for diagnosis of Sjögren's syndrome - ScienceDirect | AUTOIMMUNITY | Scoop.it
The presence of autoantibodies is one of several hallmarks of Sjögren's Syndrome, the detection of serum autoantibodies has a central role in the diag…
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Cytokines and Inflammatory Mediators in Systemic Lupus Erythematosus

Cytokines and Inflammatory Mediators in Systemic Lupus Erythematosus | AUTOIMMUNITY | Scoop.it
Systemic lupus erythematosus (SLE) is an autoimmune disease characterised by a breakdown in immune tolerance that induces an attack on normal tissue
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Epigenetic alterations in primary Sjögren's syndrome – an overview - ScienceDirect

Epigenetic alterations in primary Sjögren's syndrome – an overview - ScienceDirect | AUTOIMMUNITY | Scoop.it
Primary Sjögren's syndrome (pSS) is a chronic autoimmune rheumatic disease characterized by inflammation of exocrine glands, mainly salivary and lacri…
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"The Role of Antibody Subclass in the Pathogenesis of Pemphigus vulgari" by Eric Milan Mukherjee

A marvel of evolution, the adaptive immune system has the capacity to respond to almost any foreign antigen in a highly specific manner. Antibodies, Y-shaped glycoproteins containing both diverse variable regions responsible for antigen binding and constant regions responsible for effector...
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What role do immune cells play in dry eye?

What role do immune cells play in dry eye? | AUTOIMMUNITY | Scoop.it
Dry eye and inflammation that arise from disruption of moisturizing oil glands in the eyelids could be due to blockage by immune cells, a new study finds.
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Anti-Insulin B Cells Are Poised for Antigen Presentation in Type 1 Diabetes

Anti-Insulin B Cells Are Poised for Antigen Presentation in Type 1 Diabetes | AUTOIMMUNITY | Scoop.it
Early breaches in B cell tolerance are central to type 1 diabetes progression in mouse and man. Conventional BCR transgenic mouse models (VH125.Tg NOD) reveal the power of B cell specificity to drive disease as APCs.
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Antibody blockade of IL-15 signaling has the potential to durably reverse vitiligo

Antibody blockade of IL-15 signaling has the potential to durably reverse vitiligo | AUTOIMMUNITY | Scoop.it
In vitiligo, autoreactive T cells attack melanocytes, leading to white spots on the skin. Depigmentation typically recurs upon cessation of treatment, so new therapies are needed for permanent patient relief.
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Pancreatic islets communicate with lymphoid tissues via exocytosis of insulin peptides

Pancreatic islets communicate with lymphoid tissues via exocytosis of insulin peptides | AUTOIMMUNITY | Scoop.it
A sensitive T cell tracking assay reveals immunogenic activity of specific catabolized peptide fragments of insulin and their effects on T cell activity in lymph nodes, highlighting communication between pancreatic islets and lymphoid tissue.

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Mouse models of lupus: what they tell us and what they don’t

Lupus is a complex heterogeneous disease characterised by autoantibody production and immune complex deposition followed by damage to target tissues. Animal models of human diseases are an invaluable tool for defining pathogenic mechanisms and testing of novel therapeutic agents. There are perhaps more applicable murine models of lupus than any other human disease. There are spontaneous models of lupus, inducible models of lupus, transgenic-induced lupus, gene knockout induced lupus and humanised mouse models of lupus. These mouse models of lupus have contributed significantly to our knowledge of the pathogenesis of lupus and served as valuable preclinical models for proof of concept for new therapies. Despite their utility, mouse models of lupus have their distinct limitations. Although similar, mouse and human immune systems are different and thus one cannot assume a mechanism for disease in one is translatable to the other. Efficacy and toxicity of compounds can vary significantly between humans and mice, also limiting direct translation. Finally, the heterogeneous aspects of human lupus, both in clinical presentation, underlying pathogenesis and genetics, are not completely represented in current mouse models. Thus, proving a therapy or mechanism of disease in one mouse model is similar to proving a mechanism/therapy in a limited subset of human lupus. These limitations, however, do not marginalise the importance of animal models nor the significant contributions they have made to our understanding of lupus.
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Immunosuppressive treatment for proliferative lupus nephritis - Tunnicliffe, DJ - 2018 | Cochrane Library

Immunosuppressive treatment for proliferative lupus nephritis - Tunnicliffe, DJ - 2018 | Cochrane Library | AUTOIMMUNITY | Scoop.it
Cochrane Database of Systematic Reviews Abstract available in Background Cyclophosphamide, in combination with corticosteroids, has been first‐line treatment for inducing disease remission for proliferative lupus nephritis, reducing death at five years from over 50% in the 1950s and 1960s to less than 10% in recent years. Several treatment strategies designed to improve remission rates and minimise toxicity have become available. Treatments, including mycophenolate mofetil (MMF) and calcineurin inhibitors, alone and in combination, may have equivalent or improved rates of remission, lower toxicity (less alopecia and ovarian failure) and uncertain effects on death, end‐stage kidney disease (ESKD) and infection. This is an update of a Cochrane review first published in 2004 and updated in 2012. Objectives Our objective was to assess the evidence and evaluate the benefits and harms of different immunosuppressive treatments in people with biopsy‐proven lupus nephritis. The following questions relating to management of proliferative lupus nephritis were addressed: 1) Are new immunosuppressive agents superior to or as effective as cyclophosphamide plus corticosteroids? 2) Which agents, dosages, routes of administration and duration of therapy should be used? 3) Which toxicities occur with the different treatment regimens? Search methods We searched the Cochrane Kidney and Transplant Specialised Register up to 2 March 2018 with support from the Cochrane Information Specialist using search terms relevant to this review. Studies in the Specialised Register are identified through searches of CENTRAL, MEDLINE, and EMBASE, conference proceedings, the International Clinical Trials Register (ICTRP) Search Portal and ClinicalTrials.gov. Selection criteria Randomised controlled trials (RCTs) and quasi‐RCTs comparing any immunosuppressive treatment for biopsy‐proven class III, IV, V+III and V+VI lupus nephritis in adult or paediatric patients were included. Data collection and analysis Data were abstracted and the risks of bias were assessed independently by two authors. Dichotomous outcomes were calculated as risk ratio (RR) and measures on continuous scales calculated as mean differences (MD) with 95% confidence intervals (CI). The primary outcomes were death (all causes) and complete disease remission for induction therapy and disease relapse for maintenance therapy. Evidence certainty was determined using GRADE. Main results In this review update, 26 new studies were identified, to include 74 studies involving 5175 participants overall. Twenty‐nine studies included children under the age of 18 years with lupus nephritis, however only two studies exclusively examined the treatment of lupus nephritis in patients less than 18 years of age. Induction therapy Sixty‐seven studies (4791 participants; median 12 months duration (range 2.5 to 48 months)) reported induction therapy. The effects of all treatment strategies on death (all causes) and ESKD were uncertain (very low certainty evidence) as this outcome occurred very infrequently. Compared with intravenous (IV) cyclophosphamide, MMF may have increased complete disease remission (RR 1.17, 95% CI 0.97 to 1.42; low certainty evidence), although the range of effects includes the possibility of little or no difference. Compared to IV cyclophosphamide, MMF is probably associated with decreased alopecia (RR 0.29, 95% CI 0.19 to 0.46; 170 less (129 less to 194 less) per 1000 people) (moderate certainty evidence), increased diarrhoea (RR 2.42, 95% CI 1.64 to 3.58; 142 more (64 more to 257 more) per 1000 people) (moderate certainty evidence) and may have made little or no difference to major infection (RR 1.02, 95% CI 0.67 to 1.54; 2 less (38 less to 62 more) per 1000 people) (low certainty evidence). It is uncertain if MMF decreased ovarian failure compared to IV cyclophosphamide because the certainty of the evidence was very low (RR 0.36, 95% CI 0.06 to 2.18; 26 less (39 less to 49 more) per 1000 people). Studies were not generally designed to measure ESKD. MMF combined with tacrolimus may have increased complete disease remission (RR 2.38, 95% CI 1.07 to 5.30; 336 more (17 to 1048 more) per 1000 people (low certainty evidence) compared with IV cyclophosphamide, however the effects on alopecia, diarrhoea, ovarian failure, and major infection remain uncertain. Compared to standard of care, the effects of biologics on most outcomes were uncertain because of low to very low certainty of evidence. Maintenance therapy Nine studies (767 participants; median 30 months duration (range 6 to 63 months)) reported maintenance therapy. In maintenance therapy, disease relapse is probably increased with azathioprine compared with MMF (RR 1.75, 95% CI 1.20 to 2.55; 114 more (30 to 236 more) per 1000 people (moderate certainty evidence). Multiple other interventions were compared as maintenance therapy, but patient‐outcome data were sparse leading to imprecise estimates. Authors' conclusions In this review update, studies assessing treatment for proliferative lupus nephritis were not designed to assess death (all causes) or ESKD. MMF may lead to increased complete disease remission compared with IV cyclophosphamide, with an acceptable adverse event profile, although evidence certainty was low and included the possibility of no difference. Calcineurin combined with lower dose MMF may improve induction of disease remission compared with IV cyclophosphamide, but the comparative safety profile of these therapies is uncertain. Azathioprine may increase disease relapse as maintenance therapy compared with MMF. Plain language summary available in Immunosuppressive treatment for people with proliferative lupus nephritis What is the issue? In lupus, the body’s immune system for fighting infection attacks different parts of the body, including the kidneys. About half of all people with lupus have kidney problems. An estimated one in every 10 people who have lupus kidney disease (lupus nephritis) can develop kidney failure. The goal of treatment is to protect kidney function and avoid side‐effects. While the life expectancy of patients who have lupus has dramatically improved, available treatments can cause serious side effects such as hair loss, serious infection, and infertility. It is important to know about which treatments help to treat lupus while causing the fewest side‐effects. What did we do? We searched the Cochrane Kidney and Transplant Specialised Register up to 2 March 2018 and we combined all studies testing treatments aimed to control the body’s immune system for lupus nephritis. What did we find? In this review update, 74 studies involving 5175 patients with lupus nephritis could be studied. Treatments included intravenous (given through a vein) cyclophosphamide, oral (tablets by mouth) mycophenolate mofetil (MMF), azathioprine, and tacrolimus (used alone or together with MMF). We also found studies of treatments called “biologic” therapies, that have been designed to change very specific parts of the body’s immune system that cause it to attack itself. We looked particularly at key outcomes such as whether treatment prevented patients from needing dialysis and controlled the lupus damage to the kidney tissue (called remission). We also looked at serious side‐effects including death, infection, infertility, and hair loss. After combining the available studies, compared with cyclophosphamide, MMF may be better at getting the lupus damage to the kidneys under control. However, the range where the actual effect may suggest that MMF may make little or no difference to disease remission compared to treatment with cyclophosphamide. MMF treatment given with tacrolimus may lead to more disease remission. MMF may result in less hair loss and worse diarrhoea, but we were not certain whether MMF reduces infertility or other serious side effects. MMF was better than azathioprine for preventing kidney disease in the longer term. None of the studies told us whether treatment had any effect on death or need for dialysis, and there was very low certainty of evidence for the use of biologics in patients with lupus nephritis. Conclusions Patients with lupus nephritis may have similar or slightly better outcomes when treated with MMF or MMF with tacrolimus compared to those patients who receive intravenous cyclophosphamide. We are still not certain which is the best treatment for lupus nephritis to protect against needing dialysis in the longer term. 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Via Krishan Maggon
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Laminin 511 is a target antigen in autoimmune pancreatitis

Laminin 511 is a target antigen in autoimmune pancreatitis | AUTOIMMUNITY | Scoop.it
Autoimmune pancreatitis (AIP) is difficult to diagnose and can sometimes be confused with pancreatic cancer, which presents with similar symptoms. AIP is an inflammatory disease involving elevated IgG4, but the target autoantigen(s) is unidentified. This group’s previous work pointed to the extracellular matrix, and now, Shiokawa et al . show that a truncated form of laminin 511 may be a major autoantigen in AIP. They observed that half of AIP patients they analyzed had anti–laminin 511 antibodies, which were absent in healthy controls. Patient pancreatic tissues were positive for laminin 511, and immunization of mice with this protein induced AIP-like symptoms. These results reveal an autoimmune target in this disease and one day may aid AIP diagnosis.

Autoimmune pancreatitis (AIP), a major manifestation of immunoglobulin G4–related disease (IgG4-RD), is an immune-mediated disorder, but the target autoantigens are still unknown. We previously reported that IgG in patients with AIP induces pancreatic injuries in mice by binding the extracellular matrix (ECM). In the current study, we identified an autoantibody against laminin 511-E8, a truncated laminin 511, one of the ECM proteins, in patients with AIP. Anti–laminin 511-E8 IgG was present in 26 of 51 AIP patients (51.0%), but only in 2 of 122 controls (1.6%), by enzyme-linked immunosorbent assay. Because truncated forms of other laminin family members in other organs have been reported, we confirmed that truncated forms of laminin 511 also exist in human and mouse pancreas. Histologic studies with patient pancreatic tissues showed colocalization of patient IgG and laminin 511. Immunization of mice with human laminin 511-E8 induced antibodies and pancreatic injury, fulfilling the pathologic criteria for human AIP. Four of 25 AIP patients without laminin 511-E8 antibodies had antibodies against integrin α6β1, a laminin 511 ligand. AIP patients with laminin 511-E8 antibodies exhibited distinctive clinical features, as the frequencies of malignancies or allergic diseases were significantly lower in patients with laminin 511-E8 antibodies than in those without. The discovery of these autoantibodies should aid in the understanding of AIP pathophysiology and possibly improve the diagnosis of AIP.
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CRACR2A-Mediated TCR Signaling Promotes Local Effector Th1 and Th17 Responses

CRACR2A-Mediated TCR Signaling Promotes Local Effector Th1 and Th17 Responses | AUTOIMMUNITY | Scoop.it
Ca2+ release–activated Ca2+ channel regulator 2A (CRACR2A) is expressed abundantly in T cells and acts as a signal transmitter between TCR stimulation and activation of the Ca2+/NFAT and JNK/AP1 pathways. CRACR2A has been linked to human diseases in numerous genome-wide association studies and was shown to be one of the most sensitive targets of the widely used statin drugs. However, the physiological role of CRACR2A in T cell functions remains unknown. In this study, using transgenic mice for tissue-specific deletion, we show that CRACR2A promotes Th1 responses and effector function of Th17 cells. CRACR2A was abundantly expressed in Th1 and Th17 cells. In vitro, deficiency of CRACR2A decreased Th1 differentiation under nonpolarizing conditions, whereas the presence of polarizing cytokines compensated this defect. Transcript analysis showed that weakened TCR signaling by deficiency of CRACR2A failed to promote Th1 transcriptional program. In vivo, conditional deletion of CRACR2A in T cells alleviated Th1 responses to acute lymphocytic choriomeningitis virus infection and imparted resistance to experimental autoimmune encephalomyelitis. Analysis of CNS from experimental autoimmune encephalomyelitis–induced mice showed impaired effector functions of both Th1 and Th17 cell types, which correlated with decreased pathogenicity. Collectively, our findings demonstrate the requirement of CRACR2A-mediated TCR signaling in Th1 responses as well as pathogenic conversion of Th17 cells, which occurs at the site of inflammation.

This article is featured in In This Issue , p.[1107][1]

[1]: /lookup/volpage/201/1107
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Epigenetic alterations in primary Sjögren's syndrome – an overview - ScienceDirect

Epigenetic alterations in primary Sjögren's syndrome – an overview - ScienceDirect | AUTOIMMUNITY | Scoop.it
Primary Sjögren's syndrome (pSS) is a chronic autoimmune rheumatic disease characterized by inflammation of exocrine glands, mainly salivary and lacri…
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Full text? by elsevier

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Altered Function of Antigen-Presenting Cells in Type 1 : A Challenge for Antigen-Specific Immunotherapy?

Altered Function of Antigen-Presenting Cells in Type 1 : A Challenge for Antigen-Specific Immunotherapy? | AUTOIMMUNITY | Scoop.it
Type 1 diabetes (T1D) arises from a failure to maintain tolerance to specific β-cell antigens. Antigen-specific immunotherapy (ASIT) aims to reestablish immune tolerance through the supply of pertinent antigens to specific cell types or environments that are suitable for eliciting tolerogenic...
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Serum levels of B-cell activating factor of the TNF family (BAFF) correlate with anti-Jo-1 autoantibodies levels and disease activity in patients with anti-Jo-1positive polymyositis and dermatomyos...

Serum levels of B-cell activating factor of the TNF family (BAFF) correlate with anti-Jo-1 autoantibodies levels and disease activity in patients with anti-Jo-1positive polymyositis and dermatomyos... | AUTOIMMUNITY | Scoop.it
B-cell activating factor of the tumour necrosis factor family (BAFF) plays a role in autoantibody production and is elevated in dermatomyositis (DM) and anti-Jo-1-positive polymyositis (PM). We investigated the inter-relationships between serum levels of BAFF, anti-Jo-1 autoantibodies, and disease...
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Role of properdin in complement-mediated kidney diseases. - PubMed - NCBI

Role of properdin in complement-mediated kidney diseases. - PubMed - NCBI | AUTOIMMUNITY | Scoop.it
Nephrol Dial Transplant. 2018 Jul 19. doi: 10.1093/ndt/gfy233.[Epub ahead of print]...
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Sjögren’s syndrome - Autoimmunity

Sjögren’s syndrome - Autoimmunity | AUTOIMMUNITY | Scoop.it
Autoimmune diseases (ADs) represent a broad spectrum of chronic conditions that may afflict specific target organs or multiple systems and impose a significant burden on quality of life. The etiology of ADs is multifactorial in which a mosaic of factors (i.e., genetic, hormonal, and environmental) work in concert to induce a loss of tolerance and subsecuent tissue damage (1).
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In Vitro Diagnostics (IVD) and Laboratory Developed Tests for Autoimmune Diseases Market - Sales Ove

The growing research in human genomics is likely to play a key role in the development of the global in vitro diagnostics and laboratory developed tests for autoimmune diseases market in the coming years.
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not for content, for maps

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C-terminal truncation of IFN-γ inhibits proinflammatory macrophage responses and is deficient in autoimmune disease

IFN-γ is central in inflammatory pathogenesis, response to infection and autoimmune diseases. Here the authors show that MMP12 expression is reduced in patients with SLE and that MMP12 post-translationally truncates IFN-y, inhibiting its function and affecting pathogenesis of mouse models of peritonitis, SLE and rheumatoid arthritis.
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Frontiers | Natural Autoantibodies: An Undersugn Hero of the Immune System and Autoimmune Disorders—A Point of View | Immunology

Natural autoantibodies form a network that serves to protect the organism from outer and inner danger but also contributes to autoimmune disease. It is our view, that this critical component of the immune system deserves much greater attention than it currently attracts for the benefit of patients and for better understanding how immunity operates. Since the early days of immunology, pioneering work by Landsteiner and his group on haptens showed that immunization is a process that can raise highly specific antibodies. In the same era, Ehrlich put forward the dogma of “horror autotoxicus”, proclaiming the inability of the immune system to recognize self-constituents. Later on, in the 1950s, Burnet build upon these seminal observations and formulated the clonal selection theory which states that “cell clones produce highly specific antibodies for environmental constituents while the immune system is educated during ontogeny not to recognize self-constituents”. Nevertheless, other studies, contradicting the “dogma”, were mostly ignored. These studies showed that circulating antibodies in normal human sera could recognize various substances, including self-antigens, albeit with a low avidity 1. In the following years, additional experiments reinforced the notion of a persistent immune system reactivity against self e.g. in either normal or lupus-prone mice where the genetic background alone drives the immune system to generate IgM-producing cells that secret self-reactin
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Autoimmune septin-5 cerebellar ataxia

Autoimmune septin-5 cerebellar ataxia | AUTOIMMUNITY | Scoop.it
To report a form of autoimmune cerebellar ataxia in which antibodies target septin-5, a guanosine triphosphate (GTP)-binding neural protein involved in neurotransmitter exocytosis.Archived sera and CSF specimens with unclassified synaptic antibodies were ...
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Swiss Medical Weekly - Excipients: not so inert? When the excipient plays the role of an active substance, as exemplified by systemic lupus

Swiss Medical Weekly - Excipients: not so inert? When the excipient plays the role of an active substance, as exemplified by systemic lupus | AUTOIMMUNITY | Scoop.it
The choice of excipients is central in the drug development process. A bad choice of excipient can modify or masking the effect of the active substance. Some so-called excipients display bioactivity themselves, which can lead to unwanted effects in patients.

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