DAF/CD55 and Protectin/CD59 modulate adaptive immunity and disease outcome in experimental autoimmune myasthenia gravis
Journal of Neuroimmunology, ISSN: 0165-5728, Vol: 244, Issue: 1, Page: 63-69
2012
- 12Citations
- 22Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations12
- Citation Indexes12
- 12
- CrossRef10
- Captures22
- Readers22
- 22
Article Description
The role of regulators of complement activity (RCA) involving CD55 and CD59 in the pathogenesis of experimental autoimmune myasthenia gravis (EAMG) remains unclear. CD55 and CD59 restrict complement activation by inhibiting C3/C5 convertases' activities and membrane attack complex formation, respectively. Actively immunized EAMG mice deficient in either CD55 or CD59 showed significant differences in adaptive immune responses and worsened disease outcome associated with increased levels of serum cytokines, modified production of acetylcholine receptor antibodies, and more complement deposition at the neuromuscular junction. We conclude that modulation of complement activity by RCA represents an alternative in controlling of autoimmune processes in EAMG.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0165572812000045; http://dx.doi.org/10.1016/j.jneuroim.2012.01.003; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84857918435&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/22325826; https://linkinghub.elsevier.com/retrieve/pii/S0165572812000045; http://www.jni-journal.com/article/S0165-5728(12)00004-5/abstract; http://linkinghub.elsevier.com/retrieve/pii/S0165572812000045; http://linkinghub.elsevier.com/retrieve/articleSelectPrefsTemp?Redirect=http://jni-journal.com/retrieve/pii/S0165572812000045
Elsevier BV
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