A new report by University of Pittsburgh researchers sheds important light on how our immune systems detect invading organisms to be destroyed and removed from our bodies. Authors of the study include:
- McGowan Institute for Regenerative Medicine
faculty member Timothy Billiar, M.D. (pictured top), the George Vance Foster professor and chair in the department of surgery and also a deputy director in the Molecular Medicine Institute, and
- McGowan Institute for Regenerative Medicine affiliated faculty member Jie Fan, M.D. (pictured bottom), associate professor of surgery at the University of Pittsburgh School of Medicine.
The information from this research should ultimately help lead to the development of new drugs and treatments that allow health care providers to prevent runaway immune reactions that can have devastating consequences for people.
"Our study helps us to understand exactly how the immune system is activated when it comes across infection from bacteria or viruses," said Melanie Scott, M.D., Ph.D., another author of the research report from the Pitt’s department of surgery. "The more information we have about how this process works, the more likely we are to be able to help our immune systems fight off attacks from infections."
To make this discovery, scientists examined the production of a specific part of the complement system (called "factor B") in macrophages, an immune cell that both attacks foreign invaders and marks them for death by other types of immune cells. The researchers wanted to know if a molecule found on the outside of bacteria (lipopolysaccharide) or a synthetic version of a molecule found in some viruses (polyI:C) would stimulate factor B production by macrophages. The levels of factor B produced inside the cell were measured, as was the amount released from the cell. Results showed that lipopolysaccharide used a specific receptor on the outside of cells (TLR4) to produce factor B. polyI:C also stimulated factor B production in macrophages, not through its specific cell surface receptor (TLR3) but through another receptor that is located within cells. This shows that bacteria and viruses can produce similar end results in activating the body's defense systems, but they use different pathways to do the activation.
"As this research shows, the immune system is incredibly complex. It also highlights the redundancy which is vital to our survival," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "Viruses and bacteria have evolved many strategies to avoid immune responses, but the immune system counters with additional tricks and alternative pathways. This research helps us better understand one very important set of redundant pathways that regulates a key defense mechanism and identifies therapeutic targets for controlling that response."
Illustration: McGowan Institute for Regenerative Medicine.
Infection Control Today (09/30/10)
Science Daily (10/01/10)
Bio: Dr. Timothy Billiar
Bio: Dr. Jie Fan
Abstract (Journal of Leukocyte Biology. 2010 Oct;88(4):609-18)