Our understanding of how the host immune response influences the risk of de
veloping disease has changed dramatically over the past decade. Previously,
the spectrum of disease associated with lymphatic filariasis was largely a
ttributed to the nature of the host immune response. Now, we appreciate tha
t the duration and intensity of infection and possibly the direct influence
of parasite-derived molecules also determine the risk of disease. Individu
als chronically infected with lymphatic filariasis generally have an impair
ed lymphocyte proliferation response to filarial antigens and favour Th2-ty
pe cytokine responses. This ability to down-modulate the host immune respon
se may help protect the host from disease. Defects in antigen-presenting ce
ll (APC) function appear to participate in this acquired immune hyporespons
iveness, although the mechanisms as to how this occurs are poorly understoo
d. Here, we present evidence that repeated exposure to infective stage larv
ae and their secreted products may stimulate basophils and mast cells to re
lated products that may impair APC function.