Michael C. Carroll, Ph.D.

Title
Professor of Pediatrics; Head, Graduate Program in Immunology
Department
Immune Disease Institute
Institution
Boston Children's Hospital, Harvard University
Address
200 Longwood Ave.
WAB, Room 251
City, State, Zip
Boston, MA 2115
Phone
(617) 713-8700
E-mail
Michael.carroll[at]childrens.harvard.edu
Website
http://www.idi.harvard.edu/investigators_research/investigator/carroll_lab/
Research Field
Immunology
Award Year
1986

Research

My lab is interested in understanding the role of the complement system in innate and acquired immunity and how it links the two systems via cell surface receptors. Innate immunity is the host’s first line of defense in recognition and response to non-self. While it is often referred to as a primitive immune system (relative to acquired immunity), it includes serum proteins (such as natural IgM) and receptors (such as Toll like receptors), which are highly specific for many pathogens (and certain self-antigens). In acquired immunity, the complement system plays a critical role by marking antigen with a cleavage product of complement C3. Covalent attachment of this ligand to antigen is important for at least two reasons: (i) it enhances localization of antigen to the lymphoid compartment; (ii) it provides a ligand for B cell co-receptor which is essential for an effective B cell response. We focus on three main areas of basic research: (i) autoimmunity; (ii) inflammation; and (iii) host response to pathogens. Using genetic techniques, we develop novel strains of mice bearing altered innate or acquired immunity for study. Results from our studies of mouse models of systemic lupus erythematosus suggest that innate immunity is protective against autoimmune disease. The underlying mechanism, we believe, is due to a regulatory role of innate immunity (including complement) on tolerance of B lymphocytes.