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Jennifer Wang's Lab Sheds New Light on the Relationship Between Viral Infections and Type 1 Diabetes

Date Posted: Thursday, October 28, 2021

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A newly published study conducted in the laboratory of physician-scientist Jennifer Wang, MD, investigated the relationship between viral infections and type 1 diabetes (T1D).  Strong immune responses are activated by viral infections.  Viruses that have been associated with T1D include enteroviruses such as Coxsackievirus.  The Wang Lab continues to conduct extensive research using a unique rat model of T1D to study viruses as a possible trigger of the disease. 

“Diabetes in our rats share similarities with hallmarks of the human disease, including lack of sex bias and juvenile onset,” said Dr. Wang, Professor of Medicine in the Division of Infectious Diseases and Immunology.  “My lab is exploring whether we can protect against diabetes onset by altering the levels of innate and adaptive immune cells before disease development.”

The study, published in ImmunoHorizons, was led by postdoc Natasha Qaisar, PhD, defined how deleting components of the innate immune antiviral response alters immune cells to protect against autoimmunity. The innate immune system produces important antiviral cytokines, including type I interferon (IFN) that binds to receptors on cell surfaces to limit viral infection, providing the first line of defense.  Type I IFN has essential roles in inflammation, immunoregulation and T-cell responses and has been linked to beta-cell autoimmunity and T1D development.

For the study, Dr. Wang’s lab used a model in which viral infection triggered diabetes in rats.  The removal of type I IFN signaling resulted in dynamic shifts in innate and adaptive immune cells.  They demonstrated how this protects the rats from disease, providing insights how type I IFN drives autoimmunity.   

“We’re working to define immune cell processes that precede the damaging of beta cells by the immune system,” added Dr. Wang.  “Understanding the process leading to autoimmune responses to viral infections will pave the way to the development of approaches to prevent the onset of T1D.”

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