For us Th17 immune cells seem to be the ones that produce the out of control inflammation and the "cytokine storms" that can be so damaging.
Cytokine storms happen when our immune cells release too many and too much of several kinds of inflammatory cytokines (immune signals) which drive our defensive cells into a frenzy of destruction. This frenzy can cause these normally helpful cells to damage or kill the person they are supposed to defend.
Apparently having too many TH17 cells is a primary cause of at least some of these inflammatory cytokine storms. The importance of blocking IL-17 the seemingly 'master' inflammatory cytokine that drives inflammation as been know since at least 2003.
Currently creating a monoclonal to use therapeutically in autoimmune arthritis is a goal of the research community, and big pharma.
If you are interested in Eli Lily's Rheumatoid Arthritis phase II study of its anti IL-17 compound read here:
The study is currently enrolling patients as of December 2009. Study locations are here:
Here basic research on TB leads to answers in autoimmune disease. Let's keep funding basic research at high levels. Information gleaned leads to quicker cures for all of us.
NYU Langone Medical Center / New York University School of Medicine
New pathway discovered that may prevent tissue damage resulting from inflammation
Study could pave the way for new treatments for immune diseases
(New York, New York – December 22, 2009): Interferon gamma is a protein secreted by lymphocytes that is used to fight the bacteria in white blood cells that cause tuberculosis. In a study published this week in Immunity, scientists at NYU Langone Medical Center have discovered that in addition to white blood cells, other cells such as epithelial and endothelial cells, also respond to interferon gamma and also protect mice from uncontrolled tuberculosis infection. This new pathway could lead to the developments of treatments that could limit or prevent tissue damage resulting from inflammation.
"Through research on tuberculosis, we discovered a new way that the immune system response is controlled," said lead author Joel Ernst, MD, director of the Division of Infectious Diseases and the Jeffrey Bergstein Professor of Medicine at NYU Langone Medical Center. "Further study may reveal treatments that could be useful in control of inflammation and tissue damage in certain infections and autoimmune diseases."
In this study, researchers looked at interferon gamma responses in epithelial and endothelial cells to control tuberculosis in mice. Cells such as epithelial and endothelial cells were found to respond to interferon gamma by producing an enzyme, indolelamine-2-3-dioxygenase (IDO), that converts the amino acid tryptophan to products called kynurenines. These kynurenines inhibit the production of Th17 cells, the lymphocytes that contribute to tissue-damaging inflammation.
The study's co-author is Ludovic Desvignes, PhD of the Department of Microbiology at NYU Langone Medical Center. The research was funded by grants from the National Institute of Allergy and Infectious Diseases of the National Institutes of Health in Bethesda, Maryland.
About NYU Langone Medical Center
NYU Langone Medical Center is one of the nation's premier centers of excellence in healthcare, biomedical research, and medical education. For over 168 years, NYU physicians and researchers have made countless contributions to the practice and science of health care. Today the Medical Center consists of NYU School of Medicine, including the Smilow Research Center, the Skirball Institute of Biomolecular Medicine, and the Sackler Institute of Graduate Biomedical Sciences; the three hospitals of NYU Hospitals Center, Tisch Hospital, a 705-bed acute-care general hospital, Rusk Institute of Rehabilitation Medicine, the first and largest facility of its kind, and NYU Hospital for Joint Diseases, a leader in musculoskeletal care; and such major programs as the NYU Cancer Institute, the NYU Child Study Center, and the Hassenfeld Children's Center for Cancer and Blood Disorders.