FYI New Immune Cell Found to be a Key to Inflammatory Diseases

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A long way off a solution, but may hold future promise.

Cris______________________________________________________________New Immune Cell Found to be a Key to Inflammatory DiseasesHOUSTON - The molecular roots of inflammatory and autoimmune diseases suchas asthma, arthritis, and multiple sclerosis (MS) have been discovered by ateam of researchers led by The University of Texas M. D. CancerCenter. They say their findings may point to ways to effectively treat thesediseases ? if not stop them before they start.In a lead article in the November issue of Nature Immunology (releasedonline on Oct. 2), the scientists report finding a novel type of "T helper"cell they say is the culprit for initiating chronic inflammation andautoimmunity in a variety of body tissues. This newly described T cell ?which they call inflammatory TH cells (or THi) ? produces interleukin 17(IL-17), a potent cytokine that researchers have already linked to an immunesystem gone awry."We suspected that IL-17 is a player in autoimmune and inflammatorydiseases, but we didn't understand where IL-17 came from before thisfinding," says the study's lead investigator, Chen Dong, Ph.D., an associateprofessor in the Department of Immunology."Now we have discovered the source of IL-17 and also have solidlydemonstrated that these are the crucial cells that regulate tissueinflammation in autoimmune disease and asthma," he says. "These findingssuggest that shutting down the activity of these THi cells might stopchronic inflammatory diseases from developing in the first place."He adds that while such drugs are years away from development and clinicaltrials, agents that block IL-17 could represent an effective treatment,based on these results.Dong and four other M. D. researchers collaborated with scientistsfrom the University of Washington, the Institute for Systems Biology inSeattle and s Hopkins School of Medicine.While the findings have no immediate relevance to the field of oncology, itis known that cancer can arise from inflammatory processes. Furtherunderstanding of how the immune system functions, and how it can go awry, isimportant, Dong says.T cells are white blood cells that play a variety of roles in the immunesystem, including the identification of foreign molecules in the body, suchas bacteria and viruses, and the activation and deactivation of other immunecells.T helper cells are specific T cells that have receptors that recognize andbind to fragments (known as antigens) of the invaders that already have beendisplayed on the surface of other immune system cells. (These T helper cellsare also called CD4 T cells since they express CD4 molecules.) Once theantigen has been bound, these T helper cells become activated, and theymorph into "effector" cells which then boost an immune response by secreting"cytokine" molecules such as interleukins and interferons.Before this study, two such different types of effector T helper cells hadbeen known ? type I (TH1), linked to the body's response to microbialinfection, and type 2 (TH2), which plays a crucial function in production ofB cell antibodies and also is associated with development of allergies.Although TH1 and TH2 are known to produce powerful cytokines ? such asinterferon-gamma (IFN-g) and allergy-associated interleukin 4 (IL-4),respectively - they are not inflammatory or associated with production ofIL-17, which sets off an errant immune response that results in tissueinflammation.Researchers could not understand the origins of such an inflammatoryresponse in body tissues. The only clue they had was that excess IL-17molecules are found in arthritic joints, in lungs swollen by asthma and inbrain cells that lead to nerve degeneration and the onset of MS. "But wedidn't know which T cells were responsible for secreting IL-17," Dong says.To find out where IL-17 came from, the researchers designed a series of cellculture studies and mouse experiments. In brief, they "educated" T helpercells to become IL-17 producing cells. They found that IL-17 is triggered bya unique set of signals that now define this new "lineage" of T helpercells. "They are completely different from TH1 and TH2 effector cells," saysDong.They then used a mouse model of MS and demonstrated that they could stopdevelopment of the disease with an antibody agent that blocked IL-17.Finally, they developed a transgenic mouse model of asthma and found that,by producing excessive IL-17 in the lung, they were able to produceasthmalike symptoms.Dong says the researchers hypothesize that these newly discovered THi cellstravel to selected body tissues and release IL-17. This action, in turn,stimulates expression of "chemokines," which results in a rush ofinflammatory cells into the tissue. Thus a chronic inflammatory reaction isset up, he says.The scientists don't know what initially sets off activation of the newlydiscovered T helper cell in diseases such as arthritis and asthma, Dongsays. "We don't know why these dangerous helper T cells are activated in thepatients, but we now know how they function, and that should take us a longway to understanding and treating these and other inflammatory andautoimmune diseases."The study was funded by grants from the National Institutes of Health, theArthritis Foundation, the Cancer Research Institute and M. D. Cancer Center.Dong's co-authors include Heon Park, Ph.D., Zhaoxia Li, M.D., Ph.D., andYing Wang from the University of Washington; Leroy Hood, Ph.D., and QiangTian, Ph.D., from the Institute for Systems Biology; Zhou Zhu, M.D., Ph.D.,from s Hopkins School of Medicine; and Xuexian O. Yang, Ph.D., Seon HeeChang, Ph.D., Roza Nurieva, Ph.D., and Yi-Hong Wang, M.D., from M. D. Cancer Center.

Cris KerrAdministrator'Case Health - Health Success Stories' websiteURL: www.casehealth.com.au & www.casehealth.comWebsite Email: Online formatAustralia

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