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    Type I Interferon Signaling Is Required for Dacryoadenitis in the Nonobese Diabetic Mouse Model of Sjogren Syndrome

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    Author
    Chaly, Y; Barr, JY; Sullivan, DA; Thomas, HE; Brodnicki, TC; Lieberman, SM
    Date
    2018-10-01
    Source Title
    International Journal of Molecular Sciences
    Publisher
    MDPI
    University of Melbourne Author/s
    Thomas, Helen; Brodnicki, Thomas
    Affiliation
    Medicine and Radiology
    Metadata
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    Document Type
    Journal Article
    Citations
    Chaly, Y., Barr, J. Y., Sullivan, D. A., Thomas, H. E., Brodnicki, T. C. & Lieberman, S. M. (2018). Type I Interferon Signaling Is Required for Dacryoadenitis in the Nonobese Diabetic Mouse Model of Sjogren Syndrome. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 19 (10), https://doi.org/10.3390/ijms19103259.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/253168
    DOI
    10.3390/ijms19103259
    Abstract
    Nonobese diabetic (NOD) mice spontaneously develop lacrimal and salivary gland autoimmunity similar to human Sjögren syndrome. In both humans and NOD mice, the early immune response that drives T-cell infiltration into lacrimal and salivary glands is poorly understood. In NOD mice, lacrimal gland autoimmunity spontaneously occurs only in males with testosterone playing a role in promoting lacrimal gland inflammation, while female lacrimal glands are protected by regulatory T cells (Tregs). The mechanisms of this male-specific lacrimal gland autoimmunity are not known. Here, we studied the effects of Treg depletion in hormone-manipulated NOD mice and lacrimal gland gene expression to determine early signals required for lacrimal gland inflammation. While Treg-depletion was not sufficient to drive dacryoadenitis in castrated male NOD mice, chemokines (Cxcl9, Ccl19) and other potentially disease-relevant genes (Epsti1, Ubd) were upregulated in male lacrimal glands. Expression of Cxcl9 and Ccl19, in particular, remained significantly upregulated in the lacrimal glands of lymphocyte-deficient NOD-severe combined immunodeficiency (SCID) mice and their expression was modulated by type I interferon signaling. Notably, Ifnar1-deficient NOD mice did not develop dacryoadenitis. Together these data identify disease-relevant genes upregulated in the context of male-specific dacryoadenitis and demonstrate a requisite role for type I interferon signaling in lacrimal gland autoimmunity in NOD mice.

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