Our understanding of how the host immune response influences the risk of developing disease has changed dramatically over the past decade. Previously, the spectrum of disease associated with lymphatic filariasis was largely attributed to the nature of the host immune response. Now, we appreciate that the duration and intensity of infection and possibly the direct influence of parasite-derived molecules also determine the risk of disease. Individuals chronically infected with lymphatic filariasis generally have an impaired lymphocyte proliferation response to filarial antigens and favour Th2-type cytokine responses. This ability to down-modulate the host immune response may help protect the host from disease. Defects in antigen-presenting cell (APC) function appear to participate in this acquired immune hyporesponsiveness, although the mechanisms as to how this occurs are poorly understood. Here, we present evidence that repeated exposure to infective stage larvae and their secreted products may stimulate basophils and mast cells to related products that may impair APC function.