Sjögren’s Syndrome (SS)

My laboratory studies the autoimmune disease Sjögren’s syndrome (SS).  The mechanisms underpinning SS etiology and the corresponding early and sustained molecular events in SS disease are poorly understood.  This lack of understanding is frustrating for both clinicians and patients alike, as many individuals struggle with symptoms of disease for years before a definitive diagnosis is rendered. Significantly, there are no early markers to identify SS onset and no methods to stage the disease once diagnosis is confirmed.  While lymphocytic infiltration of salivary tissue has been studied in depth, the events responsible for lymphocyte migration to this tissue are not well characterized.  Although it is clear that aberrant activation of adaptive immunity in SS is a hallmark of disease, this must be preceded and accompanied by other pathological processes.  Early events related to dysfunction of innate immune molecules are described in mouse models of SS and innate immune dysregulation is also implicated in human SS, although the contribution of the innate immunity to disease development remains poorly understood.  Innate immune-mediated events may represent novel therapeutic targets in the treatment of SS. My laboratory is interested in the role of a specific adaptor molecule in SS, termed MyD88.  MyD88 is required for signaling by most Toll-like receptors, Interleukin-1 (IL-1) and IL-18.  Understanding how these events contribute to the development and progression of SS may enable us to develop new therapeutics that target MyD88-mediated inflammation. Early detection and subsequent mitigation of initiating events are critical to improve the quality of life for patients suffering with chronic pathoses such as SS.