Mechanistic Similarities between Antigenic Variation and Antibody Diversification during Trypanosoma brucei Infection

Abstract

Trypanosoma brucei, which causes African trypanosomiasis, avoids immunity by periodically switching its surface composition. The parasite is coated by 10 million identical, monoallelically expressed variant surface glycoprotein (VSG) molecules. Multiple distinct parasites (with respect to their VSG coat) coexist simultaneously during each wave of parasitemia. This substantial antigenic load is countered by B cells whose antigen receptors (antibodies or immunoglobulins) are also monoallelically expressed, and that diversify dynamically to counter each variant antigen. Here we examine parallels between the processes that generate VSGs and antibodies. We also discuss current insights into VSG mRNA regulation that may inform the emerging field of Ig mRNA biology. We conclude by extending the parallels between VSG and Ig to the protein level.

Keywords: African trypanosomiasis; B cell; Trypanosoma brucei; antibody; antigenic variation; immunity.