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Citation
Okuda, K., Tong, M., Dempsey, B., Moore, K.J., Gazzinelli, R.T., Silverman, N. (2016). Leishmania amazonensis Engages CD36 to Drive Parasitophorous Vacuole Maturation.  PLoS Pathog. 12(6): e1005669.
FlyBase ID
FBrf0232610
Publication Type
Research paper
Abstract

Leishmania amastigotes manipulate the activity of macrophages to favor their own success. However, very little is known about the role of innate recognition and signaling triggered by amastigotes in this host-parasite interaction. In this work we developed a new infection model in adult Drosophila to take advantage of its superior genetic resources to identify novel host factors limiting Leishmania amazonensis infection. The model is based on the capacity of macrophage-like cells, plasmatocytes, to phagocytose and control the proliferation of parasites injected into adult flies. Using this model, we screened a collection of RNAi-expressing flies for anti-Leishmania defense factors. Notably, we found three CD36-like scavenger receptors that were important for defending against Leishmania infection. Mechanistic studies in mouse macrophages showed that CD36 accumulates specifically at sites where the parasite contacts the parasitophorous vacuole membrane. Furthermore, CD36-deficient macrophages were defective in the formation of the large parasitophorous vacuole typical of L. amazonensis infection, a phenotype caused by inefficient fusion with late endosomes and/or lysosomes. These data identify an unprecedented role for CD36 in the biogenesis of the parasitophorous vacuole and further highlight the utility of Drosophila as a model system for dissecting innate immune responses to infection.

PubMed ID
PubMed Central ID
PMC4900624 (PMC) (EuropePMC)
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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    PLoS Pathog.
    Title
    PLoS Pathogens
    Publication Year
    2005-
    ISBN/ISSN
    1553-7366 1553-7374
    Data From Reference