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Min Chen, PhD

Associate Professor

Baylor College of Medicine

Pathology and Immunology


Mitochondrial autophagy in the control of systemic autoimmunity

SLE, however, the functional significance of this finding is not yet established. Interestingly, T cells from SLE patients have been found to be resistant to the induction of autophagy. SLE T cells harbor increased mitochondrial contents, leading to dysregulated mitochondrial functions and increased autoimmune potential in T cells. Whether increased mitochondrial accumulation is caused by defective autophagy is not determined. We found that knockouts of two Bcl-2 family members that regulate mitochondrial autophagy, Nix and Bnip3, resulted in abnormal T cell activation and the development of systemic autoimmune responses. We hypothesize that autophagy of mitochondria is essential for mitochondrial quality control in T cells, while defects in this process leads to abnormal T cell activation and the induction of systemic autoimmunity. We propose the following studies to test this hypothesis: 1. To test the hypothesis that defective mitochondrial autophagy leads to abnormal T cell activation; 2. To test the hypothesis that deficiency in defective mitochondrial autophagy in T cells leads to development of autoimmunity in vivo; and 3. To examine the molecular mechanisms for Nix and Bnip3 in mediating mitochondrial autophagy in T cells.

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