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Immunoregulation in Experimental Autoimmune Myasthenia Gravis—about T Cells, Antibodies, and Endplates
Author(s) -
BAETS M.,
STASSEN M.,
LOSEN M.,
ZHANG X.,
MACHIELS B.
Publication year - 2003
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1254.033
Subject(s) - myasthenia gravis , antibody , immunology , neuromuscular junction , autoimmune disease , medicine , autoimmunity , biology , neuroscience
A bstract : Experimental autoimmune myasthenia gravis (EAMG) can be induced in a large number of animal species by active immunization (AI) AChR, by passive transfer (PT) of anti‐AChR antibodies, by autologous bone marrow transplantation and cyclosporin (BMT‐Cy), or spontaneously. Depending on the model used, different immunological mechanisms are operational. In the AI model, the T cell is pivotal in directing the anti‐AChR antibody production towards pathogenic, that is, cross‐linking and complement‐fixing antibodies. Injection of anti‐AChR antibodies alone suffices to induce EAMG, excluding the role of specific cell‐mediated immune responses in the effector phase of the disease. Aged animals are resistant to the induction of AI and PT EAMG. This resistance is localized at the postsynaptic membrane containing more AChR‐anchoring proteins, including S‐laminin and rapsyn in aged animals. In BMT‐CyA EAMG, a dysregulation of the immune system in the absence of immunization is capable of inducing myasthenia. The role of these animal models in relation to pathogenesis and immunotherapy is discussed.