The aim of my research is to understand the immune responses which happen after rotavirus infection of diabetes-prone mice and to determine how these contribute to the development of T1D. Using this mouse model, I have linked specific immune responses of rotavirus infection with the development of T1D.
Importantly, these specific immune responses could be used to determine why children at high-risk of developing T1D show increased autoimmunity following rotavirus infection. This research has wider implications not only for understanding the role of viral infections in T1D development but also the role that rotavirus infection may play in other autoimmune diseases.
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