Intracellular parasites living within the harsh environment of phagocytes have developed strategies permitting their rapid physiological adaptation, escape from first-line defense systems, and the capacity to inhibit several functions of their host cells. This review has addressed some of the mechanisms by which Leishmania achieves this by manipulating signaling pathways of the host macrophage. Such strategies to manipulate the host immune response are by no means unique to Leishmania. There is increasing evidence that a great number of unicellular and pluricellular pathogens have also evolved means to inactivate or exacerbate immune cell functions, contributing to their survival and the development of pathogen-specific pathologies. It is also likely that mechanistic details will differ, sometimes markedly, between promastigotes and amastigotes and also between different species of Leishmania. These differences are likely to be of great importance in explaining the widely different clinical manifestations of leishmaniasis. However, it is clear that the common trait of these modulations is the manipulation of the host cell signaling system. As signaling pathways can be pharmacologically manipulated, a better knowledge of their role and the mechanisms whereby they regulate host immune cell functions and pathogen growth should permit the development of new therapies to control infectious agents.
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