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  1. Autoimmunity
  2. Year: 2013, Volume: 46
  3. Year: 2013, Volume: 46, Issue: 2
  4. Critical role of activation induced cytidine deaminase in Experimental Autoimmune Encephalomyelitis
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Year: 2015, Volume: 48
Year: 2014, Volume: 47
Year: 2013, Volume: 46
Year: 2013, Volume: 46, Issue: 8
Year: 2013, Volume: 46, Issue: 6
Year: 2013, Volume: 46, Issue: 3
Year: 2013, Volume: 46, Issue: 2
Regulation of Aicda expression and AID activity
Somatic Mutagenesis in Autoimmunity
Potential roles of Activation-Induced cytidine Deaminase in promotion or prevention of autoimmunity in humans
Critical role of activation induced cytidine deaminase in Experimental Autoimmune Encephalomyelitis
AID in aging and autoimmune diseases
Year: 2013, Volume: 46, Issue: 1
Year: 2012, Volume: 45
Year: 2011, Volume: 44
Year: 2010, Volume: 43
Year: 2009, Volume: 42
Year: 2008, Volume: 41
Year: 2007, Volume: 40
Year: 2004, Volume: 37
Year: 2002, Volume: 35
Year: 1994, Volume: 19
Year: 1992, Volume: 12

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Critical role of activation induced cytidine deaminase in Experimental Autoimmune Encephalomyelitis

Content Provider PubMed Central
Author Sun, Yonglian Peng, Ivan Senger, Kate Kajal, Hamidzadeh Reichelt, Mike Baca, Miriam Yeh, Ronald Lorenzo, Maria N. Sebrell, Andrew Cruz, Christopher Dela Tam, Lucinda Corpuz, Racquel Wu, Jiansheng Sai, Tao Merone, Roose-girma Warming, Søren Balazs, Mercedesz Gonzalez, Lino C. Patrick, Caplazi Martin, Flavius Devoss, Jason Zarrin, Ali A.
Copyright Year 2013
Abstract Multiple Sclerosis (MS) is a neurodegenerative autoimmune disorder caused by chronic inflammation and demyelination within the central nervous system (CNS). Clinical studies in MS patients have demonstrated efficacy with B cell targeted therapies such as anti-CD20. However, the exact role that B cells play in the disease process is unclear. Activation Induced cytidine deaminase (AID) is an essential enzyme for the processes of antibody affinity maturation and isotype switching. To evaluate the impact of affinity maturation and isotype switching, we have interrogated the effect of AID-deficiency in an animal model of MS. Here, we show that the severity of experimental autoimmune encephalomyelitis (EAE) induced by the extracellular domain of human myelin oligodendrocyte glycoprotein (MOG1-125) is significantly reduced in Aicda deficient mice, which, unlike wild-type mice, lack serum IgG to myelin associated antigens. MOG specific T cell responses are comparable between wild-type and Aicda knockout mice suggesting an active role for antigen experienced B cells. Thus affinity maturation and/or class switching are critical processes in the pathogenesis of EAE.
Related Links http://dx.doi.org/10.3109/08916934.2012.750301
Ending Page 167
Page Count 11
Starting Page 157
File Format PDF
ISSN 08916934
e-ISSN 1607842X
Journal Autoimmunity
Issue Number 2
Volume Number 46
Language English
Publisher Informa Healthcare
Publisher Date 2013-03-01
Access Restriction Open
Rights Holder Informa Healthcare
Subject Keyword Immunology Immunology and Allergy Research in Higher Education
Content Type Text
Resource Type Article
Subject Immunology and Allergy Immunology
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