Th1-like responses to peptides from peripheral nerve myelin proteins in patients with polyneuropathy associated with monoclonal gammopathy

Polyneuropathy associated with monoclonal gammopathy is usually regarded as an immune-mediated disorder with autoantibody activity against myelin glycoproteins. The pathogenic mechanisms are, however, not fully understood. Several reports have indicated an additional involvement of T cells. We investigated the occurrence of myelin-specific T cells as well as their functional characteristics. Cytokine responses generated after stimulation of peripheral blood mononuclear cells with selected peptides of myelin proteins P0 and P2 were investigated with an ELISPOT method. Three PO peptides caused significantly elevated levels of interferon-gamma (IFN-gamma)-secreting cells in patients with polyneuropathy associated with monoclonal gammopathy (n=8) compared with controls (n=8), whereas none of the peptides caused elevated levels of IL-4-secreting cells. Patients with nonimmunological types of neuropathy (n=4) did not reveal any cytokine responses to myelin peptides. Our results indicate that a Th1-like response against myelin proteins occurs in polyneuropathy associated with monoclonal gammopathy.