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Bibliographies thématiques / Autoantigeni / Livres

Livres sur le sujet « Autoantigeni »

Pour voir les autres types de publications sur ce sujet consultez le lien suivant : Autoantigeni.

Auteur : Grafiati

Publié le 11 mars 2023

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1

Martin, Alberto. Epitope studies on the human autoantigen, histidyl-tRNA synthetase. Ottawa : National Library of Canada, 1994.

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2

Brand, Stephen Robert. Autoantigenic and structural analysis of the proliferating cell nuclear antigen. Manchester : University of Manchester, 1993.

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3

Davies, Marie Louise. Autoantigen specific T cell responses in relation to systemic lupus erythematosus. Birmingham : University of Birmingham, 2000.

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4

Superoxid-Dismutase vom Mangan-Typ als Autoantigen bei akuter Epstein-Barr-Virus-Infektion. Göttingen : Cuvillier, 1996.

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5

Dumont, Caroline R. Identifying the autoantigen of a diabetogenic CD8 T cell clone isolated from Young NOD mice. [New Haven, Conn : s.n.], 1999.

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6

1953-, Eden Willem van, dir. Heat shock proteins and inflammation. Basel : Birkhäuser Verlag, 2003.

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7

Dresden Symposium on Autoantibodies (5th 2000 Dresden, Germany). Autoantigens and autoantibodies : Diagnostic tools and clues to understanding autoimmunity : report on the 5th Dresden Symposium on Autoantibodies held in Dresden on October 18-21, 2000. Lengerich : Pabst Science Publishers, 2000.

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8

S, Eisenbarth George, dir. Endocrine and organ specific autoimmunity. Austin, Tex., U.S.A : RlG. Landes Co., 1999.

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9

Winqvist, Ola. Autoantigens in Addison's Disease. Almqvist & Wiksell Internat., 1994.

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10

Frazer, Hilary Elizabeth. Autoantigens in connective tissue disease. 1986.

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11

Carton, James. Multisystem diseases. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199591633.003.0018.

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Systemic lupus erythematosus 346Systemic sclerosis 348Sarcoidosis 349Vasculitis 350• A multisystem autoimmune disease characterized by autoantibody production against a number of nuclear and cytoplasmic autoantigens.• Incidence of 4 per 100,000 people per year.• Most cases occur in women of childbearing age....

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12

Datta, Syamal Kumar, Antonio La Cava, David A. Horwitz et Ciriaco A. Piccirillo, dir. Generating and Sustaining Stable Autoantigen-specific CD4 and CD8 Regulatory T Cells in Lupus. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-788-7.

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13

Eden, Willem van. Heat Shock Proteins and Inflammation. Birkhauser Verlag, 2012.

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14

Cattran, Daniel C., et Heather N. Reich. Membranous glomerulonephritis. Sous la direction de Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.

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15

van der Vlag, Johan, et Jo H. M. Berden. The patient with systemic lupus erythematosus. Sous la direction de Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0161.

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Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with various clinical manifestations. The hallmark of SLE is the presence of antibodies against nuclear constituents, such as double-stranded (ds)DNA, histones, and nucleosomes. Local deposition of antinuclear antibodies in complex with nuclear autoantigens induces serious inflammatory conditions that can affect several tissues and organs, including the kidney.The levels of antinucleosome and anti-dsDNA antibodies seem to correlate with glomerulonephritis and these autoantibodies can often be detected years before the patient is diagnosed with SLE. Apoptotic debris is present in the extracellular matrix and circulation of patients with SLE due to an aberrant process of apoptosis and/or insufficient clearance of apoptotic cells and apoptotic debris. The non-cleared apoptotic debris in patients with SLE may lead to activation of both the innate (myeloid and plasmacytoid dendritic cells) and adaptive (T and B cells) immune system. In addition to the activation by apoptotic debris and immune complexes, the immune system in SLE may be deregulated at the level of (a) presentation of self-peptides by antigen-presenting cells, (b) selection processes for both B and T cells, and (c) regulatory processes of B- and T-cell responses. Lupus nephritis may be classified in different classes based on histological findings in renal biopsies. The chromatin-containing immune complexes deposit in the capillary filter, most likely due to the interaction of chromatin with the polysaccharide heparan sulphate. A decreased renal expression of the endonuclease DNaseI further contributes to the glomerular persistence of chromatin and the development of glomerulonephritis.Current treatment of lupus nephritis is not specific and aims to reduce the inflammatory response with general immunosuppressive therapies. However, research has revealed novel potential therapeutic candidates at the level of dendritic cells, B cells, and T cells.

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