Autoimmume and polyclonal B cell responses during murine malaria

Abstract

INTRACELLULAR protozoan infections of humans and rodents are often characterised by marked hypergamma-globulinaemia reflecting extensive activation of host B lymphocytes. In addition, the immunoglobulin (Ig) produced is directed not only against parasite antigens but also against a variety of unrelated antigenic determinants, and in some cases has been shown to contain antibodies reactive to certain host components (reviewed in refs 1 and 2). These findings have led to the suggestion that the infectious organisms may possess nonspecific or polyclonal activating properties³. Indeed, direct evidence for such mitogenic factors prepared from malarious mouse red blood cells (MRBC) has recently been obtained⁴. However, in most of these studies the use of serological or proliferative assays has provided only limited information on the different mechanisms whereby B cells are stimulated to produce antibody during the course of infection. I report here the use of plaque-forming cell (PFC) assays to reveal the patterns of both total and antigen-specific splenic B lymphocyte activation and also to define in more detail an anti-erythrocytic autoimmune response following malaria infection of mice. The results demonstrate that a specific, well-defined anti-erythrocytic response occurs shortly after infection which can be distinguished from, and induced independently of, a very large nonspecific polyclonal response. Both these responses are shown to be T-cell dependent.