Relevance of Polyclonal Antibody Formation to the Development of Autoimmunity: The Model of African Trypanosomiasis

The ability of bacterial lipopolysaccharides (LPS) to trigger the proliferation and differentiation of B lymphocytes in mice, is a well documented phenomenon (1). Administrated in conjunction with antigens, they are also powerful adjuvant of humoral immune responses (2). The possibility that LPS plays a role in the development of autoantibodies is supported by several reports (3,4). However, the precise mechanism(s) by which LPS induce the formation of autoantibodies remains unclear. It could be that LPS modulate an autoantigen driven immune response or alternatively, that LPS induce the differentiation of autoantigen reactive cells. The formation of autoantibodies with various specificities and the production by the host of large quantities of immunoglobulins have been described during African trypanosomiasis. It is therefore possible that the mechanism(s) operational in the formation of autoantibody after LPS administration are similar to those involved in the development of autoantibody seen during African trypanosomiasis. The mechanism by which LPS induce, in mice, the formation of anti-DNA and other autoantibodies has been investigated and the possible role of polyclonal B cell activation in the development of autoantibodies has been analysed during the course of African trypanosomiasis.