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Inflammatory rheostat in tuberculosis: control of tissue hypersensitivity vs tolerance to infection

Speaker: Igor Kramnik, Boston University School of Medicine

May 9, 2014 - 4:00 p.m.
Location: Fischbach Room, Folsom Library
Hosted by: Bulent Yener (x6907), Susan Gilbert (x8425)


The ability to cause destruction in the lungs of susceptible individuals is a hallmark of M.tb granulomas and a cornerstone of its virulence strategy. However, host and pathogen determinants of necrotization remain largely unknown. Using forward genetic analysis in a mouse model of TB, we have characterized a major genetic locus sst1 affecting the progression of pulmonary tuberculosis lesions and identified the Ipr1 gene within the sst1 locus using positional cloning. Analysis of the sst1/Ipr1 revealed a novel regulatory mechanism of inflammation involved in control of tissue damage caused by intracellular pathogens.


Igor Kramnik graduated from Medical School in Samara, Russia. A significant part of his clinical training focused on tuberculosis, as this disease was prevalent in his home country. He pursued research on pathogenesis of tuberculosis at the Central Institute for Tuberculosis Research in Moscow, Russia, where he studied interactions of immunocompetent cells within tuberculosis lesions using a mouse model of infection. After obtaining PhD, he moved to McGill University in Montreal, where he trained at the Centre for the Study of Host Resistance with Emil Skamene, Danuta Radzioch and Phillippe Gros focusing on mechanisms of the genetic control of host resistance to mycobacterial diseases. These studies were continued at the Albert Einstein College of Medicine in New York in the laboratory of Barry Bloom, where he characterized a mouse strain that developed necrotic tuberculosis lesions - a type of pathology characteristic of human disease, and started the genetic dissection of this phenotype. In 1999 he joined the faculty of the Department of Immunology and Infectious Diseases at the Harvard School of Public Health, where his laboratory used mouse model to further dissect mechanisms of host resistance to intracellular bacteria. Since 2009 he is an Associate Professor at the Pulmonary Center of the Department of Medicine at the BU School of Medicine and Investigator at the National Emerging Infectious Diseases Laboratory (NEIDL). His research is focused on mechanisms of immunoregulation in the lung during infections, the development of novel host directed therapies to correct susceptible phenotypes, as well as on further improvement of mouse models to test them.

Last updated: April 23, 2014