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    Macrophage Transactivation for chemokine Production identified as a negative regulator of granulomatous inflammation Using agent-Based Modeling

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    Author
    Moyo, D; Beattie, L; Andrews, PS; Moore, JWJ; Timmis, J; Sawtell, A; Hoehme, S; Sampson, AT; Kaye, PM
    Date
    2018-03-27
    Source Title
    Frontiers in Immunology
    Publisher
    FRONTIERS MEDIA SA
    University of Melbourne Author/s
    Beattie, Lynette
    Affiliation
    Microbiology and Immunology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Moyo, D., Beattie, L., Andrews, P. S., Moore, J. W. J., Timmis, J., Sawtell, A., Hoehme, S., Sampson, A. T. & Kaye, P. M. (2018). Macrophage Transactivation for chemokine Production identified as a negative regulator of granulomatous inflammation Using agent-Based Modeling. FRONTIERS IN IMMUNOLOGY, 9 (MAR), https://doi.org/10.3389/fimmu.2018.00637.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/254656
    DOI
    10.3389/fimmu.2018.00637
    Abstract
    Cellular activation in trans by interferons, cytokines, and chemokines is a commonly recognized mechanism to amplify immune effector function and limit pathogen spread. However, an optimal host response also requires that collateral damage associated with inflammation is limited. This may be particularly so in the case of granulomatous inflammation, where an excessive number and/or excessively florid granulomas can have significant pathological consequences. Here, we have combined transcriptomics, agent-based modeling, and in vivo experimental approaches to study constraints on hepatic granuloma formation in a murine model of experimental leishmaniasis. We demonstrate that chemokine production by non-infected Kupffer cells in the Leishmania donovani-infected liver promotes competition with infected KCs for available iNKT cells, ultimately inhibiting the extent of granulomatous inflammation. We propose trans-activation for chemokine production as a novel broadly applicable mechanism that may operate early in infection to limit excessive focal inflammation.

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