Immunization of rabbits with a high dose of bovine myelin results in a relapsing or progressive form of EAN . Chronic EAN has been created in the Lewis rats by immunization with myelin after treatment with low-dose cyclosporine A (CsA), which is explained by inhibition of T cell apoptosis and therefore perpetuation of inflammatory response by low-dose CsA . Higher doses of CsA actually resulted in attenuation of the disease severity, attributed to suppression of overall T cell responses, which leads to prevention of the occurrence of EAN .
Spontaneous autoimmune polyneuropathy (SAP) in nonobese diabetic (NOD) mice is another model of inflammatory neuropathy 36. The NOD mouse strain is a model of type 1 diabetes, but it also has the propensity to develop other autoimmune diseases. When B7-2 was knocked out in these mice, they did not develop insulitis and diabetes, but on the other hand, all female and one third of male mice developed a chronic demyelinating neuropathy beginning at 20 weeks of age with pathological (heavy infiltration by CD4+, CD8+ T cells and dendritic cells in peripheral nerves and dorsal root ganglia) and electrophysiological (demyelination, conduction blocking) characteristics of CIDP 129. There was overexpression of B7-1 by the antigen presenting cells in that model. The disease was reproduced by treatment of NOD mice with antibody against B7-2, and by transfer of CD4+ T cells but not by sera from SAP animals . Interferon gamma secreting Th1 cells that are reactive against certain episodes of myelin protein zero (P0) are shown to have a critical role in SAP in B7-2 deficient mouse model .