IgG STIMULATED REMYELINATION OF PERIPHERAL NERVES

Abstract

The present invention is based on the discovery of polyclonal IgG's ability to promote Schwann cell maturation, differentiation, and myelin production. Methods for treating non-idiopathic, demyelinating peripheral neuropathies in mammals, where the neuropathy is not immune-mediated or infection-mediated, through the administration of polyclonal IgG are provided. Types of demyelinating peripheral neuropathies treatable with the present invention include peripheral nerve trauma and toxin-induced peripheral neuropathies. Alternatively, a composition of polyclonal IgGs can be applied directly to a peripheral nerve cell to induce maturation, differentiation into a myelinating state, and myelin expression or promote cell survival.

1 . A method of treating i) a demyelinating peripheral neuropathy comprising administering a therapeutically effective amount of polyclonal IgG to a mammal diagnosed with said neuropathy, with the proviso that said neuropathy is not an immune-mediated or infection-mediated neuropathy and excludes Guillain-Barré syndrome, chronic demyelinating polyneuropathy and multifocal motor neuropathy, or ii) a toxin-induced peripheral neuropathy comprising administering a therapeutically effective amount of polyclonal IgG to a mammal diagnosed with said neuropathy, wherein said neuropathy is not infection-mediated. 
     
     
         2 . The method of  claim 1 , wherein the mammal is human. 
     
     
         3 . The method of  claim 1 , wherein the polyclonal IgG is administered locally. 
     
     
         4 . The method of  claim 3 , wherein the polyclonal IgG is administered intramuscularly or intradermally. 
     
     
         5 . The method of  claim 1 , wherein the polyclonal IgG is administered systemically. 
     
     
         6 . The method of  claim 5 , wherein the polyclonal IgG is administered intranasally, subcutaneously, orally, intra-arterially or intravenously. 
     
     
         7 . The method of  claim 1 , wherein an anti-inflammatory agent is co-administered with the polyclonal IgG to the mammal. 
     
     
         8 . The method of  claim 7 , wherein the anti-inflammatory agent is adrenocorticotropic hormone, a corticosteroid, an interferon, glatiramer acetate, or a non-steroidal anti-inflammatory drug. 
     
     
         9 . The method of  claim 1 , wherein the demyelinating peripheral neuropathy is selected from a trauma-induced neuropathy, a toxin-induced neuropathy, an inherited neuropathy, and a neuropathy induced by a metabolic disease. 
     
     
         10 . The method of  claim 9 , wherein the peripheral neuropathy is a trauma-induced neuropathy. 
     
     
         11 . The method of  claim 9 , wherein the peripheral neuropathy is a toxin-induced neuropathy. 
     
     
         12 . The method of  claim 9 , wherein the peripheral neuropathy is an inherited neuropathy. 
     
     
         13 .- 43 . (canceled) 
     
     
         44 . A method of promoting myelination of a peripheral nerve cell by a Schwann cell comprising contacting said Schwann cell with an amount of polyclonal IgG sufficient to promote myelination of said peripheral nerve cell by the Schwann cell. 
     
     
         45 . A method of promoting the differentiation of an immature Schwann cell into a myelinating state comprising contacting said Schwann cell with polyclonal IgG in an amount sufficient to induce the Schwann cell differentiation. 
     
     
         46 . A method of promoting the production of myelin by a Schwann cell comprising contacting said Schwann cell with an amount of polyclonal IgG sufficient to upregulate MBP genes. 
     
     
         47 . A method of culturing mammalian nervous tissue which comprises axons, said method comprising contacting the tissue in culture with an effective amount of Schwann cells and an effective amount of polyclonal IgG, whereby the contacting of Schwann cells with polyclonal IgG induces upregulation of MBP genes. 
     
     
         48 .- 49 . (canceled)