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Livres sur le sujet « IgM antibodies »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 14 février 2022

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1

Lafaille, Juan J., et Maria A. Curotto de Lafaille, dir. IgE Antibodies : Generation and Function. Cham : Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13725-4.

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2

Nelson, Paul N. Monoclonal antibodies to human IgG allotypes. Birmingham : University of Birmingham, 1988.

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3

Hanahoe, Belinda. Detection of IgG and IgE antibodies to Aspergillus fumigatus in cystic fibrosis patients. [S.l : The Author], 1993.

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4

Zhang, Xiao-Ying, Ricardo S. Vieira-Pires, Patricia M. Morgan et Rüdiger Schade, dir. IgY-Technology : Production and Application of Egg Yolk Antibodies. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72688-1.

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5

Luiten, Rosalie Margaretha. New chimeric monoclonal antibodies against human carcinomas : IgE and bispecific antibody-mediated therapy. [Leiden : University of Leiden, 1998.

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6

Sadek, Serag El Din Aly. An in vitro study of the role of IgC [inferior] 4 subclass antibodies in human anaphylactic reactions. Birmingham : University of Birmingham, 1987.

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7

Istiana. Deteksi antibodi IgG anti toxoplasma pada wanita usia subur di Kecamatan Banjarmasin Barat, Kota Banjarmasin : Tinjauan terhadap faktor umur, jumlah kehamilan, dan riwayat abortus. Banjarbaru : Fakultas Kedokteran, Universitas Lambung Mangkurat, 2008.

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8

Dörner, Thomas, et Peter E. Lipsky. Cellular side of acquired immunity (B cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0050.

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B cells have gained interest in rheumatoid arthritis (RA) beyond being the precursors of antibody-producing plasma cells since they are also a broader component of the adaptive immune system. They are capable of functioning as antigen-presenting cells for T-cell activation and can produce an array of cytokines. Disturbances of peripheral B-cell homeostasis together with the formation of ectopic lymphoid neogenesis within the inflamed synovium appears to be a characteristic of patients with RA. Enhanced generation of memory B cells and autoreactive plasma cells producing IgM-RF and ACPA-IgG antibodies together with formation of immune complexes contribute to the maintenance of RA, whereas treatment with B-cell-directed anti-CD20 therapy provides clinical benefit.

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9

Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson et Nathaniel M. Robbins. A 68-Year-Old Male with Progressive Numbness and Gait Difficulties. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0015.

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Paraproteinemic demyelinating peripheral neuropathies require specific diagnostic and management approaches. The clinical features as well as the type of monoclonal protein and possible associated antibodies are all important considerations in evaluation and management of these complex presentations. It is important to recognize anti-myelin associated glycoproteins positive peripheral neuropathy, which is associated with IgM gammopathy, and typically presents with a sensory ataxia. Hematologic disease may mimic chronic inflammatory demyelinating polyneuropathy. This chapter also describes the role of hematological evaluation for patients with peripheral neuropathy and a monoclonal gammopathy.

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10

Lafaille, Juan J., et Maria A. Curotto de Lafaille. IgE Antibodies : Generation and Function. Springer, 2016.

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11

Purdue, Mark P., Jonathan N. Hofmann, Elizabeth E. Brown et Celine M. Vachon. Multiple Myeloma. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0041.

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Multiple myeloma (MM) is the most common malignancy arising from plasma cells, fully differentiated B lymphocytes that produce the immunoglobulin (Ig) heavy- and light-chain molecules comprising antibodies. MM is characterized by an overproduction of clonal plasma cells in the bone marrow and, in most cases, monoclonal secretion of IgG, IgA, or light-chain Ig. Symptoms of end organ damage (hypercalcemia [C], renal failure [R], anemia [A], or bone lesions [B]), herein referred to as CRAB features, were traditionally a necessary criterion for diagnosing MM; however, improvements in treatment and diagnostic techniques have led to updated diagnostic criteria, enabling intervention among patients before the onset of organ damage. Multiple myeloma is an important cause of lymphoid malignancy (LM) mortality in Western populations. In the United States in 2015, MM was estimated to account for approximately one in every five newly diagnosed LMs, and one in every three LM-related deaths.

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12

Sompuram, Seshi Reddy. Purification of immunoglobulins, their bonding onto latex particles and the development of latex agglutination test for mouse IgG for monoclonal antibody assessment. 1987.

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13

(Editor), Rüdiger Schade, Ingrid Behn (Editor), Michael Erhard (Editor), Andreas Hlinak (Editor) et Christian Staak (Editor), dir. Chicken Egg Yolk Antibodies, Production and Application : IgY-Technology (Springer Lab Manuals). Springer, 2000.

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14

Lai, Kar Neng, et Sydney C. W. Tang. Immunoglobulin A nephropathy. Sous la direction de Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0069_update_001.

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A working hypothesis is that patients with immunoglobulin A (IgA) nephropathy have inherited defects in B cells producing galactose-deficient polymeric IgA1. Additional cofactors are required to form immune complexes and their deposition in glomeruli. Molecular characterization of IgG autoantibodies that recognize abnormally underglycosylated IgA1 reveals a specific amino acid substitution in the variable region of the IgG1 heavy chain. This substitution greatly enhances IgG1 binding to the galactose-deficient IgA1. The triggering antigens may include viral or bacterial antigens, or possibly by ingested food epitopes. Antiglycan IgG1 antibodies are one of the additional risk factors, or a second/multiple hit, which predisposes to disease development.

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15

Vaheri, Antti, James N. Mills, Christina F. Spiropoulou et Brian Hjelle. Hantaviruses. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0035.

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Hantaviruses (genus Hantavirus, family Bunyaviridae) are rodent- and insectivore-borne zoonotic viruses. Several hantaviruses are human pathogens, some with 10-35% mortality, and cause two diseases: hemorrhagic fever with renal syndrome (HFRS) in Eurasia, and hantavirus cardiopulmonary syndrome (HCPS) in the Americas. Hantaviruses are enveloped and have a three-segmented, single-stranded, negative-sense RNA genome. The L gene encodes an RNA-dependent RNA polymerase, the M gene encodes two glycoproteins (Gn and Gc), and the S gene encodes a nucleocapsid protein. In addition, the S genes of some hantaviruses have an NSs open reading frame that can act as an interferon antagonist. Similarities between phylogenies have suggested ancient codivergence of the viruses and their hosts to many authors, but increasing evidence for frequent, recent host switching and local adaptation has led to questioning of this model. Infected rodents establish persistent infections with little or no effect on the host. Humans are infected from aerosols of rodent excreta, direct contact of broken skin or mucous membranes with infectious virus, or rodent bite. One hantavirus, Andes virus, is unique in that it is known to be transmitted from person-to-person. HFRS and HCPS, although primarily affecting kidneys and lungs, respectively, share a number of clinical features, such as capillary leakage, TNF-, and thrombocytopenia; notably, hemorrhages and alterations in renal function also occur in HCPS and cardiac and pulmonary involvement are not rare in HFRS. Of the four structural proteins, both in humoral and cellular immunity, the nucleocapsid protein appears to be the principal immunogen. Cytotoxic T-lymphocyte responses are seen in both HFRS and HCPS and may be important for both protective immunity and pathogenesis. Diagnosis is mainly based on detection of IgM antibodies although viral RNA (vRNA) may be readily, although not invariably, detected in blood, urine and saliva. For sero/genotyping neutralization tests/RNA sequencing are required. Formalin-inactivated vaccines have been widely used in China and Korea but not outside Asia. Hantaviruses are prime examples of emerging and re-emerging infections and, given the limited number of rodents and insectivores thus far studied, it is likely that many new hantaviruses will be detected in the near future.

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Puntis, John. Food allergy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0019.

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Food allergy is an immune response to food that can be classified as immunoglobulin (Ig)-E and non-IgE mediated. Milk, egg, peanut, tree nuts, and fish are among the most prevalent causes of food allergy. Mild reactions can include itchy rash, watering eyes, and nasal congestion while a severe reaction results in anaphylaxis. A detailed clinical history is essential when making a diagnosis, and skin prick testing and quantitative measurement of food-specific IgE antibodies can be helpful. Cow milk protein allergy causes a plethora of symptoms and frequently resolves spontaneously over the first 2 years of life; diagnosis is based mainly on clinical history. Food challenges have a pivotal role in the diagnosis of food allergy. Introduction of ‘allergic’ foods at 3–6 months alongside continuing breastfeeding may prevent allergy.

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17

McKeon, Andrew. Autoimmune Encephalitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0097.

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Autoimmune encephalitis clinically encapsulates a spectrum of disorders including limbic encephalitis, and other autoimmune CNS disorders, which often have a paraneoplastic cause. Unlike multiple sclerosis, autoimmune encephalitides are unified by well-characterized neural-specific IgG biomarkers detectable in serum or CSF. Diagnostic laboratory, in vitro and neuropathological studies have demonstrated two broad groups. The first, characterizable by the detection of neuronal nuclear, cytoplasmic, or nucleolar antibodies (such as ANNA-1, aka anti-Hu), likely have a cytotoxic T cell mediated pathogenesis. The second, characterizable by the detection of antibodies targeting plasma membrane antigens, such as NMDA receptor, are likely mediated (at least in part) by pathogenic antibody.

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18

Reddy, Ugan, et Nicholas Hirsch. Diagnosis, assessment, and management of myasthenia gravis and paramyasthenic syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0244.

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Diseases that affect the neuromuscular junction (NMJ) interfere with normal nerve transmission and cause weakness of voluntary muscles. The two most commonly encountered are acquired myasthenia gravis (MG) and the Lambert–Eaton myasthenic syndrome (LEMS). Acquired MG is an autoimmune disease in which antibodies are directed towards receptors at the NMJ. In 85% of patients, IgG antibodies against the postsynaptic acetylcholine receptor (AChR) are found (seropositive MG). The thymus gland appears to be involved in the production of these which cause an increase rate of degradation of AChR resulting in a decreased receptor density resulting in a reduced postsynaptic end-plate potential following motor nerve stimulation and leading to muscle weakness. Although all voluntary muscles can be affected, ocular, bulbar, respiratory, and proximal limb weakness predominates. In the majority of seronegative patients, an antibody directed towards a NMJ protein called muscle specific tyrosine kinase (MUSK) is found. Anti-MUSK MG is characterized by severe bulbar and respiratory muscle weakness. Diagnosis of MG requires a high degree of clinical suspicion coupled with pharmacological and electrophysiological testing, and detection of the various causative antibodies. Treatment of MG involves enhancing neuromuscular transmission with long-acting anticholinesterase agents and immunosuppression. Acute exacerbations are treated with either plasma exchange or intravenous immunoglobulin. Myasthenic crisis is associated with severe muscle weakness that necessitates tracheal intubation and mechanical ventilation. LEMS is an autoimmune disease in which IgG antibodies are directed towards the pre-synaptic voltage-gated calcium channels at the NMJ. It is often associated with malignant disease (usually small cell carcinoma of the lung). Autonomic dysfunction is prominent and patients show abnormal responses to neuromuscular blocking drugs.

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19

Limaye, Vidya Sadanand. Overview and epidemiology. Sous la direction de Hector Chinoy et Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0001.

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The term idiopathic inflammatory myopathies (IIM) encompasses a heterogeneous group of muscle-dominant systemic autoimmune syndromes, including polymyositis (PM), dermatomyositis (DM), sporadic inclusion body myositis (sIBM), and immune-mediated necrotizing myopathy (IMNM). The reported incidence of IIM ranges from 5 to 10 × 10–6. Patients with PM, DM, and IMNM characteristically present with the insidious onset of symmetric proximal weakness, while in sIBM the weakness can be asymmetric, and involve the distal upper limbs and quadriceps. Dermatomyositis may also be accompanied by a range of cutaneous manifestations. Raised serum creatine kinase levels, the presence of characteristic myositis-specific antibodies, myopathic triad on electromyography, and myoedema on muscle magnetic resonance imaging are helpful in supporting a diagnosis of IIM. Muscle biopsy is the definitive diagnostic test and serves to distinguish subsets of disease, which each have characteristic histopathological changes reflecting underlying differences in pathogenesis. Mortality remains elevated in patients with IIM, despite the advent of immunosuppressive therapies.

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20

Evaluation Methods and Analytical Performance Characteristics of Immunological Assays for Human Immunoglobulin E (IGE) Antibodies of Defined Allergen. NCCLC, 1997.

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