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Relevant bibliographies by topics / Immunoglobulin A; Immunoglobulin G; Antigens / Books

Books on the topic 'Immunoglobulin A; Immunoglobulin G; Antigens'

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Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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1

Hideto, Yamada, ed. Immunoglobulin treatment in reproductive and perinatal medicine. Sapporo, Japan: Hokkaido University School of Medicine, 2002.

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2

Shakib, F. Basic and clinical aspects of IgG subclasses. Basel: Karger, 1986.

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3

Bradwell, A. R. IgG and IgA subclasses in disease. Birmingham: Binding Site, 1995.

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4

Griffiths, Helen Rosemary. Oxygen free radicals, Immunoglobulin G and rheumatoid arthritis. Birmingham: University of Birmingham, 1988.

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5

Alexander, H. Denis. An immunocytochemistry study of celular antigens and immunoglobulin heavy and light chains in leukaemia. [s.l: The Author], 1989.

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6

Nathavitharana, Kamal Augustine. Human milk and salivary secretory immunoglobulin A antibodies directed against antigens of diarrhoeagenic 'Escherichia coli'. Birmingham: University of Birmingham, 1988.

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7

United States. Animal and Plant Health Inspection Service. Veterinary Services. Centers for Epidemiology and Animal Health. Passive transfer status of heifer calves on U.S. dairies, 1991-2007. Fort Collins, CO: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services, Centers for Epidemiology and Animal Health, 2010.

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8

National Animal Health Monitoring System (U.S.) and United States. Animal and Plant Health Inspection Service. Veterinary Services., eds. Transfer of maternal immunity to calves: National Dairy Heifer Evaluation Project. Fort Collins, Colo: U.S. Dept. of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services, 1993.

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9

F, Skvaril, Morell A, and Perret B. 1944-, eds. Clinical aspects of IgG subclasses and therapeutic implications. Basel: Karger, 1988.

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10

Multifunctional IgG and IgG-binding receptors: (Ehrlich's side chain theory revisited). Amsterdam: Elsevier, 1988.

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11

David, Isenberg, and Rademacher T. W, eds. Abnormalities of IgG glycosylation and immunological disorders. Chichester: Wiley, 1996.

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12

1953-, Gordon J., ed. CD23--a novel multifunctional regulator of the immune system that binds IgE. Basel: Karger, 1991.

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13

Martin, Welschof, and Krauss Jürgen, eds. Recombinant antibodies for cancer therapy: Methods and protocols. Totowa, N.J: Humana Press, 2003.

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14

Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy. Edited by 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

F, Shakib, ed. The Human IgG subclasses: Molecular analysis of structure, function, and regulation. Oxford: Pergamon Press, 1990.

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16

Basic and Clinical Aspects of Igg Subclasses (Monographs in Allergy). Not Avail, 1986.

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17

J, Levinsky Roland, ed. IgG subclass deficiencies. London: Royal Society of Medicine Services, 1989.

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18

(Editor), John N. Abelson, Melvin I. Simon (Editor), and John J. Langone (Editor), eds. Antibodies, Antigens, and Molecular Mimicry, Volume 178: Volume 178: Antibodies, Antigens and Molecular Mimicry (Methods in Enzymology). Academic Press, 1989.

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19

Gilbert, Richard Patrick. Genetic and environmental factors affecting immunoglobulin G₁ concentrations in the colostrum and serum of ruminants. 1986.

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20

Chitko, Carol G. Sources of influence on passive and active immunoglobulin G responses in swine. 1986.

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21

Walker, Matthew R. Reactivity and specificity of monoclonal antibodies to human, immunoglobulin G constant regions and light chain variable regions. Birmingham, 1986.

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22

Webster, Michelle. Relative efficacy of intravenous immunoglobulin G in ameliorating thrombocytopenia induced by anti-platelet GPIIbIIIa versus GPIbalpha antibodies. 2006.

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23

Paul, Imbach, and Workshop on Immunoglobulin (1985 : :Lucerne, Switzerland), eds. Idiopathic thrombocytopenic purpura: Proceedings of a workshop. Chicago: PharmaLibri, 1987.

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24

Fervenza, Fernando C., An S. De Vincent Rajkumar, An S. De Vriese, and Sanjeev Sethi. Other consequences from monoclonal immunoglobulins/fragments. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0155_update_001.

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Renal damage secondary to deposition of monoclonal immunoglobulin can occur due to accumulation of either light chains, heavy chains, or both. These include myeloma kidney (cast nephropathy), light-chain and heavy-chain amyloidosis, and light- and heavy-chain deposition disease. Renal damage secondary to deposition of both chains is far less common. In the great majority of these cases the M-component is immunoglobulin G, but the spectrum of renal lesions associated with monoclonal gammopathy is extensive and depends on the physiochemical properties of the immunoglobulin produced.This chapter discusses two important, but less recognized disorders associated with monoclonal immunoglobulins: membranoproliferative glomerulonephritis and acquired Fanconi syndrome.

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25

(Editor), Martin Welschof, and Jürgen Krauss (Editor), eds. Recombinant Antibodies for Cancer Therapy: Reviews and Protocols (Methods in Molecular Biology). Humana Press, 2002.

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26

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0071.

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Antiglomerular basement membrane disease is characteristically the most rapidly progressive (crescentic) nephritis. It is often accompanied by lung haemorrhage, and occasionally causes lung disease alone. Its hallmark is linear deposition of immunoglobulin G along the glomerular basement membrane. There are usually few systemic symptoms apart from any related to the lung disease. Urine shows haematuria, often macroscopic in very acute disease.

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27

DIMMOCK, NIGEL. Neutralization Of Animal Viruses (Current Topics in Microbiology & Immunology). Springer, 1993.

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28

Barsoum, Rashad S. Schistosomiasis. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0181_update_001.

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AbstractSchistosomes are blood flukes that parasitize humans, apes, cattle, and other animals. In these definitive hosts they are bisexual, and lay eggs which are shed to fresh water where they complete an asexual cycle in different snails, ending in the release of cercariae which infect the definitive hosts to complete the life cycle.Seven of over 100 species of schistosomes are human pathogens, causing disease in different organs depending on the parasite species. Racial and genetic factors are involved in susceptibility, severity, and sequelae of infection.Morbidity is induced by the host’s immune response to schistosomal antigens. The latter include tegument, microsomal, gut, and oval antigens. The former are important in the process of invasion and establishment of infection, oval antigens in formation of granulomata which lead to fibrosis in different sites, and the gut antigens constitute the main circulating antigens in established infection, leading to immune-complex disease, particularly in the kidneys. The host immunological response includes innate and adaptive mechanisms, the former being the front line responsible for removing 90% of the infecting cercarial load. Adaptive immunity includes a Th1 phase, dominated by activation of an acute inflammatory response, followed by a prolonged Th2 phase which is responsible for immunity to re-infection as well as progression of tissue injury. Switching from Th1 to Th2 phases is controlled by functional and morphological change in the antigen-presenting cells, which is achieved by molecules of host as well as parasitic origin.Many cells participate in parasite killing, but also in the induction of tissue injury. The most potent of these is the eosinophil, which by binding antibodies to the parasite, particularly immunoglobulin E, facilitates parasite elimination. However, this process is complex, including agonist as well as antagonist pathways, which provide escape mechanisms for the parasite to survive, thereby achieving a delicate balance that permits schistosomes to live for decades in the infected host.

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29

Muche, Marion, and Seema Baid-Agrawal. Hepatitis B. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0185_update_001.

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Hepatitis B virus (HBV) has been causally linked to a variety of renal diseases, the most common being glomerular diseases and systemic autoimmune disease. Membranous nephropathy (MN) is the commonest HBV-associated glomerulonephritis (HBV-GN), followed by membranoproliferative glomerulonephritis (MPGN), mesangial proliferative glomerulonephritis, immunoglobulin (Ig)-A nephropathy, and focal segmental glomerulosclerosis (FSGS). Polyarteritis nodosa is a rare manifestation. The incidence of HBV-associated renal diseases seems to be decreasing with the introduction of vaccination programmes.HBV-MN is the most frequent cause of nephrotic syndrome in children in countries with high endemicity of HBV infection. The clinical course is usually benign in children with high rates of spontaneous remission rates and low risk of progression to renal failure. The prognosis is worse in adults. Of the systemic autoimmune disorders associated with HBV infection that involve the kidneys, the strongest link has been found with polyarteritis nodosa (PAN), a lesion that causes arteritis of medium-sized renal vessels. HBV-associated PAN (HBV-PAN) usually manifests in the first year after infection, and is clinically indistinguishable from classic PAN.Diagnosis of HBV-GN or -PAN is based on the clinical picture, histological findings, evidence of viral replication in serum and/or liver and detection of HBV antigens or DNA in the tissue. Besides deposition of immune complexes, other mechanisms such as virus-induced cytopathic damage have been proposed to explain the pathogenesis.HBV-GN and HBV-PAN appear to respond to antiviral treatment. Both show remission after HBeAg seroconversion. The available studies predominantly employed first-generation agents like interferon alpha and lamivudine, which showed suppression of viral replication and clinical remission of HBV-associated renal disease. Immunosuppressive therapy appears to be inevitable for the control of severe HBV-PAN and could be helpful in addition to antiviral treatment for cases of HBV-GN not responding clinically to antiviral treatment.

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30

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Alport post-transplant antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0075.

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Alport antiglomerular basement membrane (anti-GBM) disease is a rare example of disease caused by allo-sensitization after renal transplantation, first described in 1992. Because the recipient lacks a specific glomerular basement membrane (GBM) protein, they can become sensitized to the normal molecule present in the GBM of the donor kidney. The disease is restricted to the allograft. Interestingly severe disease arises from this only arises rarely, certainly less than 1 in 20, probably closer to 1 in 50. It characteristically causes late graft loss in a first transplant with accelerated tempo in later allografts, and in its most extreme form recurs within days. However, inexplicably some subsequent transplants do not provoke aggressive recurrence. Treatment of the most aggressive disease is difficult and in most cases has been ultimately unsuccessful. Lower levels of immune response, marked by linear binding of immunoglobulin-G to GBM without glomerular disease, are not uncommon in Alport patients after transplantation and should not lead to altered treatment. Immunoassays for anti-GBM antibodies can be misleading as in most cases the target of antibodies is the α‎‎‎5 chain of type IV collagen, rather than the α‎‎‎3 chain which is the target in spontaneous anti-GBM disease. Overall the outcome of transplantation in Alport syndrome is better than average. This complication is more likely in patients with partial or total gene deletion rather than point mutations, but no other predictive features have been identified.

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31

Morgan, Marina. Other bacterial diseasesStreptococcosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0023.

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Many pyogenic (β -haemolytic) streptococci of clinical significance have animal connections. In the last edition of this book two species of streptococci were considered of major zoonotic interest, namely Streptococcus suis and S. zooepidemicus. Since then, numerous sporadic zoonoses due to other streptococci have been reported, and a newly recognized fish pathogen with zoonotic potential termed S. iniae has emerged. Changes in nomenclature make the terminology confusing. For example, the organism known as S. zooepidemicus — now termed S. dysgalactiae subsp. zooepidemicus — still causes pharyngitis in humans, complicated rarely by glomerulonephritis after ingestion of unpasteurized milk. Pigs remain the primary hosts of S. suis with human disease mainly affecting those who have contact with pigs or handle pork.Once a sporadic disease, several major epidemics associated with high mortality have been reported in China. The major change in reports of zoonotic streptococcal infections has been the emergence of severe skin and soft tissue infections, and an increasing prevalence of toxic shock, especially due to S. suis (Tang et al. 2006), group C (Keiser 1992) and group G β -haemolytic streptococci (Barnham et al. 2002). Penicillin remains the mainstay of treatment for most infections, although some strains of group C and G streptococci are tolerant (minimum bactericidal concentration difficult or impossible to achieve in vivo) (Portnoy et al. 1981; Rolston and LeFrock 1984) and occasionally strains with increased minimum inhibitory concentrations (MIC) for penicillin are reported.Agents preventing exotoxin formation, such as clindamycin and occasionally human intravenous immunoglobulin, may be used in overwhelming infection where circulating exotoxins need to be neutralized in order to damp down the massive release of cytokines generated by their production (Darenberg et al. 2003). Prevention of human disease focuses on maintaining good hygienic practice when dealing with live animals or handling raw meat or fish products, covering skin lesions, thorough cooking of meats and pasteurization of milk.

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