NKp46+ ILC control inflammatory responses in lupus nephritis
Scientific interest within the context of the graduate college:
Our research aims to understand the role of tissue-resident cells of the innate immune system in the prevention of chronic inflammatory diseases such as systemic lupus erythematosus and inflammatory bowel disease. Our goal is to identify mechanisms that may inhibit the transition from homeostasis to chronic inflammatory disease and to determine the role of tissue-resident cells of the innate immune system in this process. Understanding such mechanisms may allow to answer the question of why some patients are susceptible to chronic autoimmune-related inflammatory diseases and others are not, and how to improve/achieve resistance to chronic inflammatory diseases.
Project description:
In Systemic Lupus Erythematosus (SLE), autoantibodies and immune complex deposition are required for pathogenesis however they are not sufficient to cause tissue damage. Tissue-specific cellular regulators that maintain tissue homeostasis and protect against inflammatory responses are largely unknown. Our overall aim in this project was to investigate the mechanisms of tissue resilience and the transition to the onset of autoimmune-induced tissue damage in the kidney. The investigated signaling pathways could reveal new therapeutic targets for patients who have already developed autoantibodies.