About Kelly Monaghan
As a graduate student in Dr. Edwin Wan’s lab, my dissertation research is focused on studying inflammation within the central nervous system resulting from the autoimmune disease multiple sclerosis. Using the murine model for MS, experimental autoimmune encephalomyelitis (EAE), we are attempting to identify downstream signaling pathways and mediators which drive inflammation and subsequent tissue damage within the CNS. Of particular interest is the cytokine GM-CSF. This cytokine is responsible for driving the differentiation and proliferation of myeloid cells, specifically dendritic cells. These cells are required to activate the autoreactive CD4+ T cells which drive EAE pathology. This cytokine will activate the signal transducer and activator of transcription a and b (STAT5) dimer, which can further oligomerize to form tetramers through their N-terminal domain. STAT5 signaling is required for controlling cell proliferation, differentiation, apoptosis and inflammation. Therefore, inhibiting total STAT5 activity is not an ideal therapeutic target. However, murine models have demonstrated that inhibiting STAT5 tetramer formation prevents the onset of EAE with minimal side effects. Therefore, we are attempting to understand the role that STAT5 tetramer formation plays in driving EAE pathology. Our ultimate goal is to selectively block STAT5 tetramer formation in order to treat MS without blocking total STAT5 activity. Outside of the lab, I am a member of the Science Policy Organization. In my free time, I enjoy yoga, exercising, hiking, reading and traveling.