Murali-Krishna Kaja, Ph.D
Associate Professor, Immunology

Department of Immunology
University of Washington
Office: H-574A, Box 357650
1959 NE Pacific Street
Seattle, WA 98195-7650
Tel: 206.221.5141
Fax: 206.543.1013
Email: mkaja@u.washington.edu

Dr. Kaja (Murali-Krishna) received his Ph.D. degree from the Indian Institute of Science, Bangalore in 1995. Following post-doctoral training in Dr. Rafi Ahmed's laboratory at Emory University, he joined the University of Washington faculty in 2001. He is an Associate Professor of Immunology and a Core Staff Faculty of Washington National Primate Center.

A hallmark of the adaptive immune system is its ability to respond with greater vigor upon second exposure to antigen. This phenomenon, termed immunological memory, is the basis of vaccination. The most efficient vaccines that we know so far are live infectious agents that are cleared following acute infection.

The goal of experiments in the Kaja laboratory is to understand the mechanisms by which innate and adaptive immune systems interact together in response to infection and generate the most efficient protective immune memory. Lessons learned from such experimental models will be useful for rational and refined vaccine design. The projects in the lab are specifically focused on understanding how type-I interferons, a set of inante anti-viral cytokines that are induced in the first few hours after infection, influence the generation and maintenance of pathogen specific cytotoxic and helper T cell responses.

Kaja Lab Members: Colin Havenar-Daughton, Graduate Student (Imm); Angela Shaulov , Graduate Student (Imm); Sunil Thomas, Ph.D. Senior Fellow ; Lucas Thompson, Graduate Student (Imm)

Representative publications:

Thomas S, Kolumam GA, Murali-Krishna K. 2007. Antigen presentation by nonhemopoietic cells amplifies clonal expansion of effector CD8 T cells in a pathogen-specific manner. J. Immunol. 178: 5802-11

Way SS, Havernar-Daughton C, Kolumam GA, Orgun NN, Murali-Krishna K. 2007. IL-12 and type-I IFN synergize for IFN-gamma production by CD4 T cells, whereas neither are required for IFN-gamma production by CD8 T cells after Listeria monocytogenes infection. J. Immunol. 178: 4498-505.

Havenar-Daughton C, Kolumam GA, Murali-Krishna K. 2006. Cutting Edge: The direct action of type I IFN on CD4 T cells is critical for sustaining clonal expansion in response to a viral but not a bacterial infection. J. Immunol. 176:3315-9.

Thompson LJ, Kolumam GA, Thomas S, Murali-Krishna K. 2006. Innate inflammatory signals induced by various pathogens differentially dictate the IFN-I dependence of CD8 T cells for clonal expansion and memory formation. J. Immunol. 177: 1746-54.

Kolumam GA, Thomas S, Thompson LJ, Sprent J, Murali-Krishna K. 2005. Type I interferons act directly on CD8 T cells to allow clonal expansion and memory formation in response to viral infection. J. Exp. Med. 202: 637-50.

Murali-Krishna K, Lau LL, Sambhara S, Lemonnier F, Altman J, Ahmed R. 1999. Persistence of memory CD8 T cells in MHC class-I deficient mice. Science 286: 1377-1381.

Murali-Krishna K, Altman J, Suresh M, Sourdive D, Zajac A, Miller J, Slansky J, Ahmed R. 1998. Counting antigen specific CD8 T cells: A re-evaluation of bystander activation during viral infection. Immunity 8: 177-187.

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Updated August 2007