The role of TLR-2, TLR-4 and MyD88 in the development of experimental autoimmune diabetes.

Author(s)

Carla Sandrina Rendall Moreira Sá

• Document type: Master's Dissertation
• Press: São Paulo.
• Institution: Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI)
• Defense date: 2013-08-14

Examining board members

Niels Olsen Saraiva Câmara; Ieda Maria Longo Maugeri; Alessandra Pontillo

• Advisor: Niels Olsen Saraiva Câmara

Abstract

Type 1 diabetes (T1D) is an autoimmune disease characterized by pancreatic beta cell destruction by activated macrophages and Th1 lymphocytes. The role of TLRs has been demonstrated in this disease, however the mechanisms involved in this process have not yet been fully explained. We evaluated the role of TLR-2, TLR-4 and MyD88 adaptor molecule in the development of experimental autoimmune diabetes induced by multiple low-doses of streptozotocin in C57Bl/6 mice. TDM1 was more severe in TLR-2 KO mice, with higher blood glucose levels and weight loss. Increased cellular infiltrate, bax and caspase-3 expression was detected in the pancreatic islets of the diabetic TLR-2 KO group suggesting a greater destruction of pancreatic cells. Interestingly, a decreased number regulatory T cells was observed in the spleen of diabetic TLR-2 KO animals. Hence, TLR-2 receptor deficiency resulted in exacerbated development of experimental autoimmune diabetes, thereby suggesting an important role for this receptor in the modulation of the immune response developed in this disease. (AU)

• FAPESP's process: 11/03833-8 - The role of Tlr-2, Tlr-4 and MyD88 in the development of experimental autoimmune diabetes
• Grantee: Carla Sandrina Rendall Moreira Sá
• Support Opportunities: Scholarships in Brazil - Master