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Published in:
2010 | OriginalPaper | Chapter
A Petri Net Model of Granulomatous Inflammation
Authors : Luca Albergante, Jon Timmis, Paul Andrews, Lynette Beattie, Paul M. Kaye
Published in: Artificial Immune Systems
Publisher: Springer Berlin Heidelberg
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Leishmania donovani
is an obligate intracellular parasite responsible for the systemic disease visceral leishmaniasis. During the course of the disease, the parasite is found in the spleen, liver and bone marrow. Characteristic of the liver immune response to leishmaniasis is a type of inflammation (“ggranulomatous inflammation”) that results in the formation of granulomas, structures comprised of an infiltrate of mononuclear cells surrounding a core of infected macrophages. Granulomas help limit the spread of infection and facilitate the killing of parasites.
Liver-resident macrophages (Kupffer cells) are able to spontaneously kill many infectious agents, but
L. donovani
is capable of reproducing inside these cells. Activation of Kupffer cells is required to turn them from host cell to a cell that is able to kill intracellular
L. donovani
. This process of activation is regulated by cytokines (notably IFN
γ
) produced by many different types of leukocytes, including natural killer (NK) cells ([1]), CD4
+
and CD8
+
T cells ([2]), and NKT cells ([3]).