Immune Disease Institute

The Davis lab researches the complement proteins of the immune system and their crucial role in the progression of hereditary angioedema and other autoimmune diseases.

Complement is an effector system activated via both the innate and adaptive immune systems. Functions that may result from complement system activation include clearance of apoptotic cells, solubilization and clearance of immune complexes, chemotaxis of inflammatory cells, opsonization of microorganisms, enhanced activation of B lymphocytes, and lysis of target cells or microorganisms.

The complement system activates blood coagulation and generates kinins that mediate enhanced vascular permeability and hypotension. These pathways are initiated by binding reactions that induce the sequential activation of a series of proteinases. These proteinases may release protein fragments with biologic activity, or may induce further protein-protein interactions that mediate subsequent activities. Proteinase regulation prevents uncontrolled activation. One important regulator is the serine proteinase inhibitor (serpin), C1 inhibitor. Its partial deficiency results in recurrent episodes of enhanced vascular permeability (hereditary angioedema) and in increased susceptibility to autoimmune disease, including systemic lupus erythematosus.

Dr. Davis graduated from the University of Illinois, Champaign-Urbana, with a degree in anthropology. He went to medical school at the University of Illinois, Chicago, and did his pediatric internship and residency at the University of Wisconsin. Then he undertook a Fellowship in Nephrology at Children's Hospital Boston, and a Fellowship in Immunology at the Center for Blood Research from 1975 until 1978. He served at Children’s Hospital Boston until 1990, when he became Director of Research in the Division of Nephrology at Children’s Hospital in Cincinnati, Ohio. In 1999 he returned to IDI as a senior investigator.