Cardiovascular disease is a major cause of increased morbidity and mortality in patients with SLE. Moreover, SLE remains an independent risk factor for cardiovascular mortality even after correction for traditional risk factor. Because treatments are often ineffective or must be discontinued due to side effects, a greater understanding of the mechanisms involved in the progression of disease is crucial to the development of more efficacious treatments. Monocytes and macrophages may be a central link between these two diseases as they are pivotal to the pathogenesis of both disease states. However the relationship between systemic inflammation, which persists in SLE, and the development of atherosclerosis is poorly understood. Thus, our goal in this predoctoral proposal is to identify potential regulators of monocyte/macrophage actions. To this end we have shown that mice lacking Bim only in myeloid cells including monocytes/macrophages develop spontaneous SLE-like disease. These data indicate that expression of Bim in myeloid cells may function as a rheostat to modulate the development of systemic autoimmunity.
|Effective start/end date||1/1/15 → 12/31/16|
- American Heart Association Midwest Affiliate (15PRE21410010)