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Targeting innate immunity in malaria
Date:8/4/2011

dy, we set out to understand what role the innate immune system plays in this fever response, the dominate symptom found in malaria patients."

Looking at blood samples from febrile malaria patients, Fitzgerald and colleagues found the typical genetic signs expected from patients infected by a pathogen. What they weren't expecting to find, however, were elevated levels of interferon-expressing genes. Typically produced when a virus is detected, interferon triggers the protective defenses of the immune system that can eradicate viruses or tumors. "What we saw when we looked at the samples from malaria patients was a type 1 interferon signature in the immune cells that were responding to the malaria," said Fitzgerald. "This surprised us at the time because traditionally we thought of interferon only in the context of virus infections"

Working with Douglas T. Golenbock, MD, chief of the Division of Infectious Diseases and Immunology at UMMS, Dr. Fitzgerald and colleagues set out to find what was triggering the innate immune response and what effect that response was having on the host cells. What they found was a part of the malaria genome containing a dense portion of the nucleic acids adenine and thymine, two of the building blocks in DNA, which were responsible for activating a novel signaling pathway, including STING, TBK1 and IRF3-IRF7, in the host that enabled innate immune cells to produce type 1 interferon.

When Fitzgerald and colleagues proceeded to test the importance of this pathway to the progression of the disease in small animal models they found another surprise. Those which expressed the normal STING, TBK1 and IRF3-IRF7 pathway all succumbed to the infection within 12 days. However, those that lacked some or all of these genes survived the infection, suggesting that this novel DNA-sensing pathway that leads to type 1 interferon production may play a vital role in the progression of malaria in the host.

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Contact: Jim Fessenden
james.fessenden@umassmed.edu
508-856-2000
University of Massachusetts Medical School
Source:Eurekalert

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