The molecular roots of inflammatory and autoimmune diseases such as asthma, arthritis, and multiple sclerosis (MS) have been discovered by a team of researchers led by the University of Texas M.D. Anderson Cancer Center.
In a lead article in the November issue of Nature Immunology (released online Oct.2nd) the scientists report finding a novel type of “T helper” cell they say is the culprit for initiating chronic inflammation and autoimmunity in a variety of body tissues.
“We suspected that IL-17 is a player in autoimmune and inflammatory diseases, but we didn’t understand where IL-17 came from before this finding,” says the study’s lead investigator, Chen Dong, Ph.D., an associate professor in the Department of Immunology. “Now we have discovered the source of IL-17 and also have solidly demonstrated that these are the crucial cells that regulate tissue inflammation in autoimmune disease and asthma.”
He adds that while such drugs are years away from development and clinical trials, agents that block IL-17 could represent an effective treatment, based on these results.
Dong and four other M.D. Anderson researchers collaborated with scientists from the University of Washington, the Institute for Systems Biology in Seattle and Johns Hopkins School of Medicine.
While the findings have no immediate relevance to the field of oncology it is known that cancer can arise from inflammatory processes.
T cells are white blood cells that play a variety of roles in the immune system, including the i.d. of foreign molecules in the body, such as bacteria and viruses, and the activation and deactivation of other immune cells.
T helper cells are specific T cells that have receptors that recognize and bind to fragments (known as antigens) of the invaders that already have been displayed on the surface of other immune system cells. (These T helper cells re also called CD4 T cells since they express CD4 molecules).
Before this study two such different types of effector T helper cells had been known – type I (TH1), linked to the body’s response to microbial infection, and type 2 (TH2), which plays a crucial function in production of B cell antibodies and also is associated with development of allergies.
Although TH1 and TH2 and known to produce powerful cytokines – such as interferon-gamma (IFN-g) and allergy-associated interleukin 4 (IL-4), respectively – they are not inflammatory or associated with production of IL-17, which sets off an errant immune response that results in tissue inflammation.
Researchers could not understand the origins of such inflammatory response in body tissues.
Dong says the researchers hypothesize that these newly discovered THi cells travel to selected body tissues and release IL-17.