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Autoimmunity Reviews Jun 2016As autoantibodies bind to target tissues, Fc-region dependent inflammation can induce pain via mediators exciting nociceptors. But recently another possibility has... (Review)
Review
As autoantibodies bind to target tissues, Fc-region dependent inflammation can induce pain via mediators exciting nociceptors. But recently another possibility has emerged, where autoantibody binding to nociceptors can directly cause pain, without inflammation. This is thought to occur as a result of Fab-region mediated modification of nerve transduction, transmission, or neuropeptide release. In three conditions, complex regional pain syndrome, anti-voltage gated potassium channel complex autoimmunity, and chronic fatigue syndrome, all associated with no or only little inflammation, initial laboratory-, and clinical trial-results have suggested a potential role for autoantibody-mediated mechanisms. More research assessing the pathogenic roles of autoantibodies in these and other chronic pain conditions is required. The concept of autoantibody-mediated pain offers hope for the development of novel therapies for currently intractable pains.
Topics: Autoantibodies; Chronic Disease; Humans; Inflammation; Neuralgia
PubMed: 26883460
DOI: 10.1016/j.autrev.2016.02.011 -
The Lancet. Rheumatology Dec 2023Increased research over the past 30 years has greatly improved the understanding of the pathophysiological mechanisms and clinical aspects of autoantibody-positive... (Review)
Review
Increased research over the past 30 years has greatly improved the understanding of the pathophysiological mechanisms and clinical aspects of autoantibody-positive rheumatoid arthritis, resulting in improved management and outcomes. In contrast, the subset of rheumatoid arthritis that does not have autoantibodies (such as rheumatoid factor and anti-citrullinated protein autoantibodies) remains less well defined in its pathogenic mechanisms. Autoantibody-negative rheumatoid arthritis continues to pose diagnostic challenges, might respond differently to therapies, and appears to be burdened with different comorbidities and outcomes. The clear separation of rheumatoid arthritis according to serotypes is still a subject of uncertainty and controversy, and studies specifically focused on comparing rheumatoid arthritis and rheumatoid arthritis-like arthritides that do not have autoantibodies remain scarce. The purpose of this Review is to summarise the peculiarities that make autoantibody-negative rheumatoid arthritis different from its autoantibody-positive counterpart, with the aim of generating debate and stimulating further research on this challenging condition.
Topics: Humans; Autoantibodies; Rheumatologists; Arthritis, Rheumatoid; Rheumatoid Factor; Anti-Citrullinated Protein Antibodies
PubMed: 38251565
DOI: 10.1016/S2665-9913(23)00242-4 -
International Journal of Molecular... Feb 2020Autoantibodies encountered in patients with systemic rheumatic diseases bear clinical significance as a biomarker to help or predict diagnosis, clinical phenotypes,... (Review)
Review
Autoantibodies encountered in patients with systemic rheumatic diseases bear clinical significance as a biomarker to help or predict diagnosis, clinical phenotypes, prognosis, and treatment decision-making. Furthermore, evidence has accumulated regarding the active involvement of disease-specific or disease-associated autoantibodies in the pathogenic process beyond simple association with the disease, and such knowledge has become essential for us to better understand the clinical value of autoantibodies as a biomarker. This review will focus on the current update on the autoantibodies of four rheumatic diseases (rheumatoid arthritis, myositis, systemic sclerosis, and anti-neutrophil cytoplasmic antibody associated vasculitis) where there has been a tremendous progress in our understanding on their biological effects and clinical use.
Topics: Antibodies, Antineutrophil Cytoplasmic; Autoantibodies; Biomarkers; Humans; Rheumatic Diseases
PubMed: 32085664
DOI: 10.3390/ijms21041382 -
Neuropediatrics Dec 2013Autoantibodies to the extracellular domain of neuronal proteins cause different neurological conditions with movement disorders as a prominent feature. We reviewed the... (Review)
Review
Autoantibodies to the extracellular domain of neuronal proteins cause different neurological conditions with movement disorders as a prominent feature. We reviewed the literature of autoantibody-mediated and autoantibody-associated diseases focusing on anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis, autoimmune basal ganglia encephalitis, Sydenham chorea, and the rare syndrome of progressive encephalomyelitis with rigidity and myoclonus. NMDAR encephalitis is a diffuse encephalitis with psychiatric and cognitive features associated with autoantibodies against the NR1 subunit of the NMDAR. The movement disorder phenotype is diverse and often generalized in young children. Although orofacial dyskinesia was the initial movement phenotype, chorea, dystonia, catatonia, and stereotypical movements are now described. The stereotypical movements can be bizarre and include cycling movements and compulsive self-injurious behavior. Autoimmune basal ganglia encephalitis is an inflammatory encephalitis localizing to the basal ganglia that is sometimes associated with serum antibodies against dopamine-2 receptor. Although psychiatric features are common, the dominant problem is a movement disorder, with dystonia-parkinsonism being characteristic. Sydenham chorea is the prototypic poststreptococcal autoimmune neuropsychiatric disorder and several autoantibodies may be involved in disease generation. The syndrome is characterized by a pure chorea, although hypotonia, dysarthria, and emotional lability are common. Progressive encephalomyelitis with rigidity and myoclonus is a rare autoimmune disorder causing rigidity, stimulus sensitive spasms, and myoclonus of nonepileptic origin and is associated with autoantibodies of multiple types including those against the glycine receptor. These disorders are important to recognize and diagnose, as immune therapy can shorten disease duration and improve outcome.
Topics: Autoantibodies; Humans; Movement Disorders
PubMed: 24203856
DOI: 10.1055/s-0033-1358603 -
Advances in Clinical Chemistry 2024Idiopathic inflammatory myopathies (IIM), generally referred to as myositis is a heterogeneous group of diseases characterized by muscle inflammation and/or skin... (Review)
Review
Idiopathic inflammatory myopathies (IIM), generally referred to as myositis is a heterogeneous group of diseases characterized by muscle inflammation and/or skin involvement, diverse extramuscular manifestations with variable risk for malignancy and response to treatment. Contemporary clinico-serologic categorization identifies 5 main clinical groups which can be further stratified based on age, specific clinical manifestations and/or risk for cancer. The serological biomarkers for this classification are generally known as myositis-specific (MSAs) and myositis-associated antibodies. Based on the use of these antibodies, IIM patients are classified into anti-synthetase syndrome, dermatomyositis, immune-mediated necrotizing myopathy, inclusion body myositis, and overlap myositis. The current classification criteria for IIM requires clinical findings, laboratory measurements, and histological findings of the muscles. However, the use MSAs and myositis-associated autoantibodies as an adjunct for disease evaluation is thought to provide a cost-effective personalized approach that may not only guide diagnosis but aid in stratification and/or prognosis of patients. This review provides a comprehensive overview of contemporary autoantibodies that are specific or associated myositis. In addition, it highlights possible pathways for the detection and interpretation of these antibodies with limitations for routine clinical use.
Topics: Humans; Autoantibodies; Myositis; Biomarkers
PubMed: 38762242
DOI: 10.1016/bs.acc.2024.04.001 -
Seminars in Pediatric Neurology Aug 2017Movement disorders secondary to autoantibodies in children represent a rapidly expanding group of conditions. Once considered to be limited to poststreptococcal... (Review)
Review
Movement disorders secondary to autoantibodies in children represent a rapidly expanding group of conditions. Once considered to be limited to poststreptococcal Sydenham's chorea or rare cases of childhood systemic lupus erythematosus, a variety of antibody-related movement abnormalities are now seen as part of noninfectious autoimmune encephalitis or within an expanding list of postinfectious disorders. In this article, several proposed autoantibody-mediated movement disorders in children are reviewed. In each one, there is a hypothesized antibody biomarker that is believed to be pathogenic and cause the clinical symptoms. As will be discussed, in some, such as anti-NMDA receptor encephalitis, the strength of supporting evidence is strong. In others, antibodies have been identified, but their role as the pathophysiological mechanism remains undetermined. Lastly, there are proposed disorders, such as PANDAS, that are controversial on both a clinical and autoimmune basis.
Topics: Autoantibodies; Child; Humans; Movement Disorders
PubMed: 29103424
DOI: 10.1016/j.spen.2017.08.003 -
Orvosi Hetilap Oct 2022Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by pathological immune complexes and various autoantibodies. Detectable pathological... (Review)
Review
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by pathological immune complexes and various autoantibodies. Detectable pathological autoantibodies produced by plasma cells differentiated from B cells play a significant role in the establishment of clinical diagnosis, classification, and differential diagnosis as well as assessing the disease activity during patients’ follow-up. Autoantibody determination is very important in
Topics: Humans; Antigen-Antibody Complex; Lupus Erythematosus, Systemic; Autoantibodies; Antibodies, Antiphospholipid; Prognosis
PubMed: 36273352
DOI: 10.1556/650.2022.32599 -
Practical Neurology Feb 2012
Review
Topics: Animals; Autoantibodies; Central Nervous System Diseases; Humans
PubMed: 22258167
DOI: 10.1136/practneurol-2011-000094 -
Best Practice & Research. Clinical... Dec 2014Autoantibodies are the serological hallmark of autoimmune disease. Though their pathogenic role is debatable, they play an important role in the management of a patient... (Review)
Review
Autoantibodies are the serological hallmark of autoimmune disease. Though their pathogenic role is debatable, they play an important role in the management of a patient with rheumatic disease. However, due to their presence in the general population as well as in multiple autoimmune diseases, the presence of an autoantibody alone does not make a diagnosis; the result has to be interpreted along with clinical findings. Similarly, the absence of autoantibody does not exclude a disease. The common autoantibodies used in clinical practice include rheumatoid factor, anti-CCP antibodies, antinuclear antibodies (ANAs), anti-neutrophil cytoplasmic antibodies (ANCA) and anti-phospholipid antibodies. Once an autoantibody to a broad antigen is detected in a patient, sub-specificity analysis can improve the utility of the antibody. Autoantibodies are detected in the serum using different assays and results of which can vary; thus, it is important for a clinician to know the method used, its sensitivity and specificity to help in the proper interpretation of the laboratory results. This review will address these issues.
Topics: Antibodies, Antinuclear; Antibodies, Antiphospholipid; Autoantibodies; Autoimmune Diseases; Humans; Rheumatic Diseases; Rheumatoid Factor; Sensitivity and Specificity
PubMed: 26096093
DOI: 10.1016/j.berh.2015.04.010 -
Science (New York, N.Y.) Feb 2024Autoantibodies influence a wide range of conditions beyond autoimmune diseases.
Autoantibodies influence a wide range of conditions beyond autoimmune diseases.
Topics: Humans; Autoantibodies; Autoimmune Diseases; Neoplasms; Antigens, Neoplasm; COVID-19; Interferon Type I
PubMed: 38359108
DOI: 10.1126/science.abn1034