Reed
Amy J. Reed, MD, Ph.D.
Instructor in Anesthesia,
Critical Care and Pain Medicine
Beth Israel Deaconess Medical Center
Harvard Medical School

330 Brookline Avenue, RN-224
Boston, MA 02215
Office: 617-667-1025
Fax: 617-667-1035
Email:
areed1@bidmc.harvard.edu

Education/Training/Appointments:

Amy J. Reed earned her M.D. and Ph.D. in Immunology from the University of Pennsylvania Medical School.  After a postdoctoral fellowship in transplant immunology, she went on to complete residency in Anesthesiology and subsequently a fellowship in Critical Care at the Hospital of the University of Pennsylvania.  She joined the Department of Anesthesia, Critical Care and Pain Medicine at Beth Israel Deaconess Medical Center in October, 2011.


Research Interests: Immunology of Sepsis

Translational Research - Sepsis and the Systemic Inflammatory Response Syndrome (SIRS) that results from abdominal trauma-related intestinal perforation and exposure of the peritoneal cavity to fecal material is a significant cause of morbidity and mortality in intensive care patients.  Sepsis is driven by an incompletely characterized systemic hyper-inflammatory response triggered by a variety of insults, most notably gram-negative bacteria and their endotoxins.  Our lab is interested in the contribution of the B cell compartment to intestinal perforation-related sepsis.  In this regard, the peritoneal cavity is uniquely populated by a subset of B cells, termed B-1 B cells, differentiating them from their more common peripheral counterparts, B-2 B cells.  B-1 B cells are not only anatomically specialized but also posses a distinct ontogeny and threshold for activation relative to B-2 B cells.  Their location and capacity to be rapidly activated to secrete anti-microbial natural antibodies makes them prime candidates for defense against abdominal sepsis.  Our lab makes use of the murine cecal ligation and puncture (CLP) model as a well-defined system that closely recapitulates the pathophysiology that occurs in abdominal trauma-related sepsis and has a similarly high mortality rate. Studies in our laboratory have demonstrated that the peritoneal immune system and, in particular B-1 B cells, undergoes rapid activation in response to peritoneal fecal contamination.  The focus of the lab is to examine the parameters that determine the activation and subsequent differentiation of B-1 cells and their ultimate role in the pathophysiology in abdominal sepsis.


New and Noteworthy Publications:

Reed AJ, Riley MP, Caton AJ. Virus-induced maturation and activation of autoreactive memory B cells. Journal of Experimental Medicine. 2000;192:1763.

Jordan MS, Boesteann A, Reed AJ, Petrone AL, Holenbeck AE, Lerman MA, Nami A, Caton AJ. Thymic selection of CD4+CD25+ regulatory T cells induced by an agonist self-peptide. Nature Immunology. 2001;2:301.

Reed AJ, Noorchasm H, Rostami SY, Zarrabi Y, Perate AR, Jeganathan AN, Caton AJ, Naji A. Alloreactive T cell activation in vivo: an autonomous function of the indirect pathway of alloantigen presentation. Journal of immunology. 2003;171:6502.

Reed AJ, Zarrabi Y, Perate AL, Jeganathan A, Naji A, Noorchasm H. The frequency of double-positive thymocytes expressing an alpha-beta TCR clonotype regulates peripheral CD4 T cell compartment homeostasis. Immunology. 2005; 116:400-407.

Rankin AL, Reed AJ, Oh S, Cozzo Picca C, Guay HM, Larkin J, 3rd, Panarey L, Aitken MK, Koeberlein B, Lipsky PE, Tomaszewski JE, Naji A, Caton AJ. CD4+ T cells recognizing a single self-peptide expressed by APCs induce spontaneous autoimmune arthritis. Journal of Immunology. 2008:180:833.