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    Neutrophils are dispensable in the modulation of T cell immunity against cutaneous HSV-1 infection

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    Author
    Hor, JL; Heath, WR; Mueller, SN
    Date
    2017-01-23
    Source Title
    Scientific Reports
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Heath, William; Mueller, Scott; HOR, JYH LIANG
    Affiliation
    Microbiology and Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    Hor, J. L., Heath, W. R. & Mueller, S. N. (2017). Neutrophils are dispensable in the modulation of T cell immunity against cutaneous HSV-1 infection. SCIENTIFIC REPORTS, 7 (1), https://doi.org/10.1038/srep41091.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258012
    DOI
    10.1038/srep41091
    Abstract
    Neutrophils rapidly infiltrate sites of inflammation during peripheral infection or tissue injury. In addition to their well described roles as pro-inflammatory phagocytes responsible for pathogen clearance, recent studies have demonstrated a broader functional repertoire including mediating crosstalk between innate and adaptive arms of the immune system. Specifically, neutrophils have been proposed to mediate antigen transport to lymph nodes (LN) to modulate T cell priming and to influence T cell migration to infected tissues. Using a mouse model of cutaneous herpes simplex virus type 1 (HSV-1) infection we explored potential contributions of neutrophils toward anti-viral immunity. While a transient, early influx of neutrophils was triggered by dermal scarification, we did not detect migration of neutrophils from the skin to LN. Furthermore, despite recruitment of neutrophils into LN from the blood, priming and expansion of CD4+ and CD8+ T cells was unaffected following neutrophil depletion. Finally, we found that neutrophils were dispensable for the migration of effector T cells into infected skin. Our study suggests that the immunomodulatory roles of neutrophils toward adaptive immunity may be context-dependent, and are likely determined by the type of pathogen and anatomical site of infection.

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