Feb. 9, 2011 So-called barrier sites -- the skin, gut, lung -- limit the inner body's exposure to allergens, pollutants, viruses, bacteria, and parasites. Understanding how the immune system works in these external surfaces has implications for understanding such inflammatory diseases as asthma, psoriasis, IBD, and food allergies, all of which occur at the body's barriers.
David Artis, PhD, professor of Microbiology at the University of Pennsylvania School of Medicine, and Gregory F. Sonnenberg, a predoctoral fellow in the Artis lab, have identified an immune cell population that acts as the body's border patrol with the outside world. They discovered that these lymphoid tissue inducer cells maintain immunity in the intestine of mice. The research appeared in the most recent online issue of Immunity.
Following infection by Citrobacter rodentium -- a model of human E. coli infection in the gut -- this cell population was the dominant source of IL-22, a molecule that helps in the immune response during the early phases of infection. When the inducer cells were eliminated from the intestine of the experimental mice, immunity was impaired, affecting the production of anti-microbial proteins required to fight infection. The mice eventually died.
This discovery could also represent a new line of research for HIV/AIDS, says Artis, since there is a breakdown of barrier immunity in the gut (a reservoir for HIV) that can lead to full blown AIDS. Therapeutics to target such immune cells could be an important new way to combat AIDS.
The research was funded by the National Institute of Allergy and Infectious Diseases, the Burroughs Welcome Fund, and the Crohn's and Colitis Foundation of America.
Other social bookmarking and sharing tools:
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
- Gregory F. Sonnenberg, Laurel A. Monticelli, M. Merle Elloso, Lynette A. Fouser, David Artis. CD4 Lymphoid Tissue-Inducer Cells Promote Innate Immunity in the Gut. Immunity, 2011; 34 (1): 122 DOI: 10.1016/j.immuni.2010.12.009
Note: If no author is given, the source is cited instead.