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Deutsches Arzteblatt International Mar 2022Pregnancies in women with chronic disease are on the rise. This pertains to autoimmune diseases in particular since these tend to affect women of childbearing age. The... (Review)
Review
BACKGROUND
Pregnancies in women with chronic disease are on the rise. This pertains to autoimmune diseases in particular since these tend to affect women of childbearing age. The interaction between pregnancy and autoimmune disease may increase the risk of maternal, fetal, and obstetric complications; additional care may be required.
METHODS
This review is based on a selective literature search in PubMed (2015-2020).
RESULTS
In women with autoimmune diseases, the course of pregnancy is highly variable. Some autoimmune diseases tend to improve during pregnancy and do not to result in any serious obstetric complications. Others may worsen during pregnancy, with deterioration of the maternal condition as well as obstetric and perinatal complications. In systemic lupus erythematosus and myasthenia gravis, placental transfer of specific autoantibodies may cause fetal or neonatal disease.
CONCLUSION
The care of pregnant women with chronic diseases requires collaboration between specialists of the pertinent levels of care. A stable course of disease before conception, close interdisciplinary care, and pregnancy-compatible medication contribute to a reduction in maternal and perinatal complications.
Topics: Autoimmune Diseases; Female; Humans; Infant, Newborn; Lupus Erythematosus, Systemic; Placenta; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Prenatal Care
PubMed: 34874264
DOI: 10.3238/arztebl.m2021.0353 -
Scandinavian Journal of Immunology Feb 2021Inflammation can be created by several different causes, including a blood clot, an immune system disorder, a cancer, an infection, a chemical exposure, a physical... (Review)
Review
Inflammation can be created by several different causes, including a blood clot, an immune system disorder, a cancer, an infection, a chemical exposure, a physical injury, or a neurological condition, such as Alzheimer's or depression. In particular, many infections by viral, bacterial, fungal and protozoan pathogens can cause inflammation. Inflammations can have far-reaching medical consequences, because chronic or frequent inflammation can assist cancers and initiate autoimmune diseases. Determining the cause of an inflammation can be essential for the medical treatment of an individual, and a classification system can be a useful tool to help a diagnosis, confirm a diagnosis and to determine the most appropriate treatment. However, at present there is no classification system for the different causes of inflammation. This paper describes a classification system that uses seven distinct cytokine parameters to enable the determination of the cause of an inflammation. This classification system is expandable, and it can help determine whether an inflammation is caused by an ischaemia, an immune system disorder, a cancer, an infection, a chemical, a physical injury, or a neurological condition. In some cases, this classification system can help enable a quick primary or secondary determination of an urgent medical emergency when other medical diagnostic resources are unavailable.
Topics: Autoimmune Diseases; Cytokines; Humans; Immune System; Inflammation
PubMed: 32892387
DOI: 10.1111/sji.12970 -
Current Opinion in Immunology Feb 2023Autoimmunity is characterized by self-reactive immune components and autoimmune disease by autoimmunity plus pathology. Both autoimmunity and autoimmune diseases are... (Review)
Review
Autoimmunity is characterized by self-reactive immune components and autoimmune disease by autoimmunity plus pathology. Both autoimmunity and autoimmune diseases are dramatically increasing in many parts of the world, likely as a result of changes in our exposures to environmental factors. Current evidence implicates the momentous alterations in our foods, xenobiotics, air pollution, infections, personal lifestyles, stress, and climate change as causes for these increases. Autoimmune diseases have a major impact on the individuals and families they affect, as well as on our society and healthcare costs, and current projections suggest they may soon take their place among the predominant medical disorders. This necessitates that we increase the scope and scale of our efforts, and coordinate our resources and studies, to understand autoimmune disease risk factors and pathogeneses and improve our diagnostic, therapeutic, and preventive approaches, as the costs of inaction will be profound and far greater without such investments.
Topics: Humans; Autoimmunity; Prevalence; Autoimmune Diseases; Air Pollution
PubMed: 36446151
DOI: 10.1016/j.coi.2022.102266 -
Multiple Sclerosis (Houndmills,... Oct 2019Myelin oligodendrocyte glycoprotein (MOG) antibody disease is a rare autoimmune disorder with antibodies against the MOG predominantly involving the optic nerve and... (Review)
Review
Myelin oligodendrocyte glycoprotein (MOG) antibody disease is a rare autoimmune disorder with antibodies against the MOG predominantly involving the optic nerve and spinal cord leading to vision loss and paralysis. When MOG antibody disease involves the brain, the phenotype is similar to acute disseminated encephalomyelitis (ADEM). In this review, we discuss MOG-positive cases presenting with encephalitis, encephalopathy, or ADEM-like presentation based on recently published series.
Topics: Adrenal Cortex Hormones; Autoantibodies; Demyelinating Autoimmune Diseases, CNS; Disease Progression; Encephalitis; Encephalomyelitis; Humans; Immunoglobulins, Intravenous; Immunologic Factors; Immunosuppressive Agents; Magnetic Resonance Imaging; Myelin-Oligodendrocyte Glycoprotein; Optic Neuritis; Plasma Exchange
PubMed: 30907249
DOI: 10.1177/1352458519837705 -
Frontiers in Immunology 2023Myasthenia gravis (MG) is a neuromuscular autoimmune disorder characterized by chronic but intermittent fatigue of the eye- and general body muscles. Muscle weakness is... (Review)
Review
Myasthenia gravis (MG) is a neuromuscular autoimmune disorder characterized by chronic but intermittent fatigue of the eye- and general body muscles. Muscle weakness is caused primarily by the binding of an autoantibody to the acetylcholine receptors, resulting in blockage of normal neuromuscular signal transmission. Studies revealed substantial contributions of different proinflammatory or inflammatory mediators in the pathogenesis of MG. Despite these findings, compared to therapeutic approaches that target autoantibody and complements, only a few therapeutics against key inflammatory molecules have been designed or tested in MG clinical trials. Recent research focuses largely on identifying unknown molecular pathways and novel targets involved in inflammation associated with MG. A well-designed combination or adjunct treatment utilizing one or more selective and validated promising biomarkers of inflammation as a component of targeted therapy may yield better treatment outcomes. This review briefly discusses some preclinical and clinical findings of inflammation associated with MG and current therapy approaches and suggest the potential of targeting important inflammatory marker(s) along with current monoclonal antibody or antibody fragment based targeted therapies directed to a variety of cell surface receptors.
Topics: Humans; Myasthenia Gravis; Receptors, Cholinergic; Autoantibodies; Muscles; Inflammation
PubMed: 36793733
DOI: 10.3389/fimmu.2023.1110499 -
Nature Genetics Oct 2020We report on the influence of ~22 million variants on 731 immune cell traits in a cohort of 3,757 Sardinians. We detected 122 significant (P < 1.28 × 10)...
We report on the influence of ~22 million variants on 731 immune cell traits in a cohort of 3,757 Sardinians. We detected 122 significant (P < 1.28 × 10) independent association signals for 459 cell traits at 70 loci (53 of them novel) identifying several molecules and mechanisms involved in cell regulation. Furthermore, 53 signals at 36 loci overlapped with previously reported disease-associated signals, predominantly for autoimmune disorders, highlighting intermediate phenotypes in pathogenesis. Collectively, our findings illustrate complex genetic regulation of immune cells with highly selective effects on autoimmune disease risk at the cell-subtype level. These results identify drug-targetable pathways informing the design of more specific treatments for autoimmune diseases.
Topics: Autoimmune Diseases; Autoimmunity; Genetic Predisposition to Disease; Genome-Wide Association Study; Humans; Italy; Phenotype; Polymorphism, Single Nucleotide
PubMed: 32929287
DOI: 10.1038/s41588-020-0684-4 -
Seminars in Cancer Biology Aug 2020Cancer and autoimmune disease are closely related, and many therapeutic antibodies are widely used in clinics for the treatment of both diseases. Among them, the... (Review)
Review
Cancer and autoimmune disease are closely related, and many therapeutic antibodies are widely used in clinics for the treatment of both diseases. Among them, the anti-CD20 antibody has proven to be effective against both lymphoid malignancy and autoimmune disease. Moreover, immune checkpoint blockade using the anti-PD1/PD-L1/CTLA4 antibody has improved the prognosis of patients with refractory solid tumors. At the same time, however, over-enhancement of immunoreaction can induce autoimmune reaction. Although anti-TNF antibody therapies represent a breakthrough in the treatment of autoimmune diseases, optimal management is required to control the serious associated issues, including development and progression of cancer, and it is becoming more and more important to control the immunoreaction. In addition, next-generation antibody therapeutics such as antibody-drug conjugates and bispecific antibodies, are anticipated to treat uncontrolled cancer and autoimmune disease. IL-7R signaling plays an important role in the development and progression of both lymphoid malignancy and autoimmune disease. In addition, abnormal homing activity and steroid resistance caused by IL-7R signaling may worsen prognosis. Therefore, anti-IL-7R targeting antibody therapies that enable suppression of such pathophysiological status have the potential to be beneficial for the treatment of both diseases. In this review, we discuss current antibody therapeutics in cancer and autoimmune disease, and describe a new therapeutic strategy for immunoregulation including IL-7R targeting antibodies.
Topics: Animals; Antibodies, Monoclonal; Antineoplastic Agents, Immunological; Autoimmune Diseases; Humans; Immunotherapy; Neoplasms; Receptors, Interleukin-7
PubMed: 31181267
DOI: 10.1016/j.semcancer.2019.06.001 -
Nature Reviews. Drug Discovery Jan 2021Despite recent advances in the treatment of autoimmune and inflammatory diseases, unmet medical needs in some areas still exist. One of the main therapeutic approaches... (Review)
Review
Despite recent advances in the treatment of autoimmune and inflammatory diseases, unmet medical needs in some areas still exist. One of the main therapeutic approaches to alleviate dysregulated inflammation has been to target the activity of kinases that regulate production of inflammatory mediators. Small-molecule kinase inhibitors have the potential for broad efficacy, convenience and tissue penetrance, and thus often offer important advantages over biologics. However, designing kinase inhibitors with target selectivity and minimal off-target effects can be challenging. Nevertheless, immense progress has been made in advancing kinase inhibitors with desirable drug-like properties into the clinic, including inhibitors of JAKs, IRAK4, RIPKs, BTK, SYK and TPL2. This Review will address the latest discoveries around kinase inhibitors with an emphasis on clinically validated autoimmunity and inflammatory pathways.
Topics: Animals; Autoimmune Diseases; Autoimmunity; Humans; Inflammation; Protein Kinase Inhibitors; Protein Kinases
PubMed: 33077936
DOI: 10.1038/s41573-020-0082-8 -
Journal of Autoimmunity May 2020Systemic autoinflammatory diseases (SAIDs) are a growing group of disorders caused by a dysregulation of the innate immune system leading to episodes of systemic... (Review)
Review
Systemic autoinflammatory diseases (SAIDs) are a growing group of disorders caused by a dysregulation of the innate immune system leading to episodes of systemic inflammation. In 1997, MEFV was the first gene identified as disease causing for Familial Mediterranean Fever, the most common hereditary SAID. In most cases, autoinflammatory diseases have a strong genetic background with mutations in single genes. Since 1997 more than 30 new genes associated with autoinflammatory diseases have been identified, affecting different parts of the innate immune system. Nevertheless, for at least 40-60% of patients with phenotypes typical for SAIDs, a distinct diagnosis cannot be met, leading to undefined SAIDs (uSAIDs). However, SAIDs can also be of polygenic or multifactorial origin, with environmental influence modulating the phenotype. The implementation of a disease continuum model combining the adaptive and the innate immune system with autoinflammatory and autoimmune diseases shows the complexity of SAIDs and the importance of new methods to elucidate molecular changes and causative factors in SAIDs. Diagnosis is often based on clinical presentation and genetic testing. The timeline from onset to diagnosis takes up to 7.3 years, highlighting the indisputable need to identify new treatment and diagnostic targets. Recently, other factors are under investigation as additional contributors to the pathogenesis of SAIDs. This review gives an overview of pathogenesis and etiology of SAIDs, and summarizes recent diagnosis and treatment options.
Topics: Animals; Autoimmune Diseases; Biomarkers; Disease Management; Disease Susceptibility; Host-Pathogen Interactions; Humans; Inflammasomes; Inflammation; Organ Specificity; Signal Transduction
PubMed: 32019685
DOI: 10.1016/j.jaut.2020.102421 -
Indian Journal of Ophthalmology Sep 2020Autoimmune retinopathy (AIR) refers to a group of rare autoimmune retinal degenerative diseases presumably caused by cross-reactivity of serum autoantibodies against... (Review)
Review
Autoimmune retinopathy (AIR) refers to a group of rare autoimmune retinal degenerative diseases presumably caused by cross-reactivity of serum autoantibodies against retinal antigens. The pathogenesis of AIR remains largely presumptive and there are a significant number of antiretinal antibodies that have been detected in association with AIR. The diagnosis of AIR is largely based on the demonstration of antiretinal antibodies in the serum along with suggestive clinical features and ancillary investigations. A high index of suspicion along with early diagnosis and treatment may play a critical role to lower the risk of irreversible immunological damage to the retinal cells in these patients. A multi-disciplinary approach for complete management and evaluation is helpful in such conditions. Various therapeutic options have been described for the treatment of AIR, though there is no consensus on standard treatment protocol.
Topics: Autoantibodies; Autoantigens; Autoimmune Diseases; Humans; Retina; Retinal Diseases
PubMed: 32823399
DOI: 10.4103/ijo.IJO_786_20