TY - JOUR
T1 - Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis
AU - Goluszko, Elzbieta
AU - Hjelmström, Peter
AU - Deng, Caishu
AU - Poussin, Mathilde A.
AU - Ruddle, Nancy H.
AU - Christadoss, Premkumar
N1 - Funding Information:
The study was supported by Muscular Dystrophy Association and Association Française Contre les Myopathies (P.C.), NIH, CA ROI CA 16885 (NHR), and a fellowship from the Swedish Foundation for International Cooperation in Research and Higher Education (P.H.). M. Poussin is a consecutive postdoctoral fellow of Association Françaisc Contre les Myopathies, Osserman fellow of the MG Foundation of America, and James W. McLaughlin Foundation postdoctoral fellow. C. Deng was an Osserman fellow of MG Fountation and James W. McLaughlin Foundation postdoctoral fellow.
PY - 2001/2/1
Y1 - 2001/2/1
N2 - A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-α deficient (LT-α-/-) mice compared to LT-α+/+ mice when immunized with acetylcholine receptor. However, only a partial prevention of clinical EAMG incidence was observed in LT-β-/- mice compared to LT-β+/+ mice. LT-α-/- and LT-β-/- mice had lower mean titers of total IgG, IgG1, IgG2a and IgG2b and higher or equal mean titers of IgM anti-AChR antibodies compared to controls. Therefore, LT-α-/- and LT-β-/- AChR immunized mice are capable of mounting a primary (IgM) humoral immune response to AChR, but are less capable of switching to the pathogenic anti-AChR IgG isotypes. LT could play a significant role in the pathogenesis of myasthenia gravis.
AB - A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-α deficient (LT-α-/-) mice compared to LT-α+/+ mice when immunized with acetylcholine receptor. However, only a partial prevention of clinical EAMG incidence was observed in LT-β-/- mice compared to LT-β+/+ mice. LT-α-/- and LT-β-/- mice had lower mean titers of total IgG, IgG1, IgG2a and IgG2b and higher or equal mean titers of IgM anti-AChR antibodies compared to controls. Therefore, LT-α-/- and LT-β-/- AChR immunized mice are capable of mounting a primary (IgM) humoral immune response to AChR, but are less capable of switching to the pathogenic anti-AChR IgG isotypes. LT could play a significant role in the pathogenesis of myasthenia gravis.
KW - Acetylcholine receptors
KW - Autoimmunity
KW - Cytokines
KW - Lymphotoxins
KW - Myasthenia gravis
KW - TNF receptors
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U2 - 10.1016/S0165-5728(00)00420-3
DO - 10.1016/S0165-5728(00)00420-3
M3 - Article
C2 - 11137582
AN - SCOPUS:0035255040
SN - 0165-5728
VL - 113
SP - 109
EP - 118
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 1
ER -