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1

Slayton, Kaetzel Charlotte, ed. Mucosal immune defense: Immunoglobulin A. New York: Springer, 2007.

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2

Slayton, Kaetzel Charlotte, ed. Mucosal immune defense: Immunoglobulin A. New York: Springer, 2007.

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3

1942-, Honjo T., Alt Frederick W e Rabbitts T. H, eds. Immunoglobulin genes. London: Academic Press, 1989.

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4

Kaushik, Azad K., e Yfke Pasman. Comparative immunoglobulin genetics. Toronto: Apple Academic Press, 2014.

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5

Lazarus, Alan H. Immunoglobulin therapy. Bethesda, Md: AABB Press, 2010.

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6

Lefranc, Marie-Paule. The immunoglobulin factsbook. San Diego: Academic Press, 2001.

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7

F, Calabi, e Neuberger, eds. Moleculargenetics of immunoglobulin. Amsterdam: Elsevier, 1987.

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8

Slayton, Kaetzel Charlotte, ed. Mucosal immune defense: Immunoglobulin A. New York: Springer, 2007.

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9

Paolo, Casali, Silberstein Leslie E e New York Academy of Sciences., eds. Immunoglobulin gene expression in development and disease. New York: New York Academy of Sciences, 1995.

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10

F, Calabi, e Neuberger M. S, eds. Molecular genetics of immunoglobulin. Amsterdam: Elsevier, 1987.

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11

Stephen, Jolles, ed. Intravenous immunoglobulin in dermatology. London: Martin Dunitz, 2003.

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12

B, Fick Robert, e Jardieu Paula M, eds. IgE and anti-IgE therapy in asthma and allergic disease. New York: Marcel Dekker, 2002.

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13

Kaetzel, Charlotte Slayton, ed. Mucosal Immune Defense: Immunoglobulin A. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-72232-0.

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14

Lundgren, Mats. Activation of immunoglobulin isotype switching. Stockholm: [s.n.], 1995.

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15

International Symposium on Immunoglobulin Subclass Deficiences (1985 Lund, Sweden). Immunoglobulin subclass deficiencies: International Symposium on Immunoglobulin Subclass Deficiencies, Lund, September 26-27, 1985. Editado por Hanson Lars Å ed, Söderström T. ed e Oxelius V. ed. Basel: Karger, 1986.

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16

Brümmendorf, Thomas. Cell adhesion molecules 1: immunoglobulin superfamily. London: Academic Press, 1994.

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17

Cooper, Max D., Toshiyuki Takai e Jeffrey V. Ravetch, eds. Activating and Inhibitory Immunoglobulin-like Receptors. Tokyo: Springer Japan, 2001. http://dx.doi.org/10.1007/978-4-431-53940-7.

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18

L, Yap P., ed. Clinical applications of intravenous immunoglobulin therapy. Edinburgh: Churchill Livingstone, 1992.

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19

Brümmendorf, Thomas. Cell adhesion molecules 1: immunoglobulin superfamily. London: Academic Press, 1995.

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20

F, Shakib, ed. Autoantibodies to immunoglobulins. Basel: Karger, 1989.

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21

Donata, Vercelli, ed. IgE regulation: Molecular mechanisms. Chichester: J. Wiley, 1997.

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22

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

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23

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

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24

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

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25

Oancea, Adriana Ecaterina. Immunoglobulin heavy chain gene expression in hybridoma cells. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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26

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

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27

C, Dalakas Marinos, ed. The use of intravenous immunoglobulin for neurologic diseases. Hagerstown, MD: Lippincott Williams & Wilkins, 1998.

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28

Royal College of Obstetricians and Gynaecologists. Use of anti-D immunoglobulin for Rh prophylaxis. London: RCOG, 1999.

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29

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

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30

Daley, Mary Denise. Molecular analysis of human immunoglobulin V[lambda] germline genes. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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31

Palmer, Jon. Selected abstracts on idiotypes, anti-idiotypes and network regulation. Bethesda, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, International Cancer Research Data Bank, National Cancer Institute, 1987.

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32

Pennycook, Jacqueline Louise Mitchell Hamilton. Analysis of endogenous immunoglobulin gene rearrangement in the SCID mouse. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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33

Waters, P. J. In Vitro and In Silico characterisation of a novel immunoglobulin. London: University of East London, 1999.

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34

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

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35

van de Winkel, Jan G. J., e P. Mark Hogarth, eds. The Immunoglobulin Receptors and their Physiological and Pathological Roles in Immunity. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5018-7.

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36

Kaetzel, Charlotte S. Mucosal Immune Defense: Immunoglobulin A. Springer London, Limited, 2007.

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37

Kaetzel, Charlotte S. Mucosal Immune Defense: Immunoglobulin A. Springer, 2010.

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38

Mucosal Immune Defense: Immunoglobulin A. Springer, 2007.

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39

Alt, Frederick W., e Tasuku Honjo. Immunoglobulin Genes. Elsevier Science & Technology Books, 2012.

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40

Alt, Frederick W., e Tasuku Honjo. Immunoglobulin Genes. Elsevier Science & Technology Books, 1995.

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41

Pasman, Yfke, e Azad K. Kaushik. Comparative Immunoglobulin Genetics. Apple Academic Press, Incorporated, 2014.

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42

Pasman, Yfke, e Azad K. Kaushik. Comparative Immunoglobulin Genetics. Taylor & Francis Group, 2021.

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43

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

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44

Lefranc, Marie-Paule, e Gerard Lefranc. Immunoglobulin FactsBook. Elsevier Science & Technology Books, 2001.

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45

Immunoglobulin Genes. Elsevier, 1995. http://dx.doi.org/10.1016/b978-0-12-053640-5.x5000-9.

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46

(Editor), T. Honjo, e F. W. Alt (Editor), eds. Immunoglobulin Genes. 2a ed. Academic Press, 1995.

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47

Mestecky, Jiri. Immunoglobulin a System. Springer London, Limited, 2013.

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48

Lai, Kar Neng, e Sydney C. W. Tang. Immunoglobulin A nephropathy. Editado por Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0065.

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Immunoglobulin A (IgA) nephropathy is the most common primary glomerulonephritis. It runs a slow and sometimes relentless clinical course with consequent end-stage renal failure in 35–40% of patients 25–30 years after first clinical presentation. The pathology is characterized by deposition of macromolecular (polymeric) IgA1 in the glomerular mesangium, proliferation of mesangial cells, increased synthesis of extracellular matrix, and infiltration of macrophage, monocytes, and T cells.
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49

Lai, Kar Neng, e Sydney C. W. Tang. Immunoglobulin A nephropathy. Editado por Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0066_update_001.

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Immunoglobulin A (IgA) nephropathy characteristically causes haematuria and may present as a nephritic illness in older children and young adults. However, it may occur at any age and is commonly asymptomatic, associated first with haematuria alone, later progressing in some patients to hypertension, proteinuria, and progressive loss of glomerular filtration. While this evolution is characteristically slow, over decades, in some it is rapid, leading to early end-stage renal failure. It is common for the disease to present late, as advanced renal disease, or malignant hypertension. It may present with acute kidney injury caused by crescentic disease, but acute kidney injury caused by haematuria may be confused clinically with the same. Henoch–Schönlein purpura is a type of small vessel vasculitis that is most commonly seen in children, but which occurs at all ages, that is associated with IgA deposition. In older children and most adults it merges closely into IgA nephropathy after the acute event. Outcomes in adults are less good. IgA nephropathy is the most common type of glomerulonephritis in most developed countries. The disease is more common in men, and appears to be much less common in black people. The detected incidence is strongly influenced by biopsy policies; the lower your threshold to biopsy patients with haematuria, the more of this condition you discover. There are clear genetic tendencies but the strongest risk seems to come from genes in the human leucocyte antigen complex.
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50

Lai, Kar Neng, e Sydney C. W. Tang. Immunoglobulin A nephropathy. Editado por Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0068_update_001.

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Immunoglobulin A nephropathy is characteristically slowly evolving, and studies from autopsies and kidney donors show that deposition of immunoglobulin A is quite common and not necessarily associated with overt disease. However, series of biopsy-diagnosed patients that extend to 20 or 30 years report rates of end-stage renal failure of up to 40–50%. A very approximate overall rate of end-stage renal disease of 1% per year has been suggested. Proteinuria, glomerular filtration rate (GFR), and possibly some features on renal biopsies enable risk stratification, but all patients need long-term monitoring. Treatment is based on the use of angiotensin converting-enzyme inhibitors for patients with proteinuria, and blood pressure control, and of course during most of the previous long-term studies patients would not have been treated with these agents or to modern blood pressure standards. For patients who show loss of GFR despite this, or other markers of high risk, the best evidence is for treatment with high-dose corticosteroids over a limited period of months. There is little convincing evidence for additional benefit from cytotoxic or other immunomodulatory agents, except possibly in the most aggressive disease, when there is weak evidence for cyclophosphamide. Some studies claim benefit from tonsillectomy, but this is not clear, and most nephrologists only recommend this for patients with recurrent tonsillitis.
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