Keratinocytes produce IL-17c to protect peripheral nervous systems during human HSV-2 reactivation

IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses

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Macrophage-Induced Blood Vessels Guide Schwann Cell-Mediated Regeneration of Peripheral Nerves

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Secreted Herpes Simplex Virus-2 Glycoprotein G Modifies NGF-TrkA Signaling to Attract Free Nerve Endings to the Site of Infection

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Alterations in the Microbiota Drive Interleukin-17C Production from Intestinal Epithelial Cells to Promote Tumorigenesis

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Keratinocyte Overexpression of IL-17C Promotes Psoriasiform Skin Inflammation

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Rapid localized spread and immunologic containment define Herpes simplex virus-2 reactivation in the human genital tract

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TLR3 deficiency renders astrocytes permissive to herpes simplex virus infection and facilitates establishment of CNS infection in mice

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Polymorphisms in Toll-like receptor 3 confer natural resistance to human herpes simplex virus type 2 infection

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Interleukin-17C Promotes Th17 Cell Responses and Autoimmune Disease via Interleukin-17 Receptor E

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IL-17RE is the functional receptor for IL-17C and mediates mucosal immunity to infection with intestinal pathogens

(2011) Xinyang Song et al.   NATURE IMMUNOLOGY

IL-17C regulates the innate immune function of epithelial cells in an autocrine manner

(2011) Vladimir Ramirez-Carrozzi et al.   NATURE IMMUNOLOGY

Daedalus: a robust, turnkey platform for rapid production of decigram quantities of active recombinant proteins in human cell lines using novel lentiviral vectors

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Mucosal host immune response predicts the severity and duration of herpes simplex virus-2 genital tract shedding episodes

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Persistence of HIV-1 receptor–positive cells after HSV-2 reactivation is a potential mechanism for increased HIV-1 acquisition

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Herpes simplex virus infection is sensed by both Toll-like receptors and retinoic acid-inducible gene- like receptors, which synergize to induce type I interferon production

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