TY - JOUR
T1 - Complement regulator CD59 deficiency fails to augment susceptibility to actively induced experimental autoimmune myasthenia gravis
AU - Tüzün, Erdem
AU - Saini, Shamsher S.
AU - Morgan, B. Paul
AU - Christadoss, Premkumar
N1 - Funding Information:
This study is supported by NIHR21A1049995, Muscular Dystrophy Association, and Advanced Technology Program of Texas Higher Education Coordinating Board.
Funding Information:
Generation and characterization of the CD59 KO mice was funded by a Programme Grant to Paul Morgan from the Wellcome Trust (Ref. 068590).
PY - 2006/12
Y1 - 2006/12
N2 - Complement deficient mice are resistant to experimental autoimmune myasthenia gravis (EAMG), suggesting a pivotal role for the membrane attack complex (MAC) in EAMG pathogenesis. To test the significance of MAC regulation in EAMG pathogenesis, CD59 KO and wild type mice were immunized with acetylcholine receptor (AChR). Interestingly, deletion of CD59, the regulator of MAC assembly, failed to augment EAMG susceptibility. The CD59 KO mice had reduced serum anti-AChR IgG1, IgG2b and complement levels. Their lymph node cell IL-2 production and lymphocyte proliferation response to AChR were reduced. The data challenge the current paradigm that CD59 is solely involved in MAC regulation and suggest a role for this molecule in antigen-driven T cell and B cell activation.
AB - Complement deficient mice are resistant to experimental autoimmune myasthenia gravis (EAMG), suggesting a pivotal role for the membrane attack complex (MAC) in EAMG pathogenesis. To test the significance of MAC regulation in EAMG pathogenesis, CD59 KO and wild type mice were immunized with acetylcholine receptor (AChR). Interestingly, deletion of CD59, the regulator of MAC assembly, failed to augment EAMG susceptibility. The CD59 KO mice had reduced serum anti-AChR IgG1, IgG2b and complement levels. Their lymph node cell IL-2 production and lymphocyte proliferation response to AChR were reduced. The data challenge the current paradigm that CD59 is solely involved in MAC regulation and suggest a role for this molecule in antigen-driven T cell and B cell activation.
KW - Autoimmunity
KW - CD59
KW - Complement
KW - Experimental autoimmune myasthenia gravis
KW - Myasthenia gravis
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U2 - 10.1016/j.jneuroim.2006.07.016
DO - 10.1016/j.jneuroim.2006.07.016
M3 - Article
C2 - 17056125
AN - SCOPUS:37849188628
SN - 0165-5728
VL - 181
SP - 29
EP - 33
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1-2
ER -