The African trypanosomes (Trypanosoma brucei sp.) are parasites of humans and domestic animals in sub-Saharan Africa, causing the disease trypanosomiasis or sleeping sickness [1]. Unlike the other parasites described in this volume these kinetoplastid protozoa are extracellular. As such, they have evolved remarkable immune-evasion mechanisms which shed light on fundamental differences between intracellular and extracellular modes of parasitism. This review will cover recent advances in the immunology of African trypanosomiasis. T. brucei is generally divided into three subspecies according to their infectivity to humans and the characteristics of the disease they cause. T. b. rhodesiense and T. b. gambiense cause sleeping sickness in man in East and West Africa respectively, while T. b. brucei is restricted to wild animal hosts due to lytic factors in human serum. Genetic evidence [2] suggests that T. b. brucei and T. b. rhodesiense are indistinguishable apart from the human infectivity trait which is itself unstable, and for the purposes of this review these subspecies will be referred to as T. brucei. Trypanosomiasis is a typical zoonosis, and the reservoir of infection in wild animals means that disease eradication is likely to be unattainable. It is estimated that there are 50 million people at risk from infection, with the reported 100,000 cases per annum likely to be a considerabe underestimate due to the lack of effective monitoring in many areas [3]. T. brucei infects laboratory rodents readily, and as a result the mouse model has been used for almost all immunological studies. Different inbred strains of mice exhibit a spectrum of resistance to T. brucei both in terms of survival time and parasitaemia. However, all eventually succumb to the parasite. Genetic analysis has shown resistance to be under polygenic control [4], but the nature of the factors involved is not known.