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<p class="publishdate"><span property="dc:date" datatype="xsd:dateTime" content="2010-11-01T00:00:00-04:00" class="date-display-single">November 1, 2010</span></p><div class='syndicate'><h1>The Origins of Autoimmunity-Causing T Cells</h1><div class="media-float-right"><div class="ds-1col file file-image file-image-jpeg view-mode-floated_media clearfix">
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-large/public/news-events/research-matters/2010/20101101-tcells.jpg?itok=-ltBx77B&timestamp=1433965068 1x" media="screen and (min-width: 960px)" />
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-medium/public/news-events/research-matters/2010/20101101-tcells.jpg?itok=eIugob4N&timestamp=1433965068 1x" media="screen and (min-width: 800px)" />
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-medium-small/public/news-events/research-matters/2010/20101101-tcells.jpg?itok=L0OwWyDF&timestamp=1433965068 1x" media="screen and (min-width: 600px)" />
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-small/public/news-events/research-matters/2010/20101101-tcells.jpg?itok=ytzXuLXW&timestamp=1433965068 1x" media="screen and (min-width: 480px)" />
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<source srcset="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-tiny/public/news-events/research-matters/2010/20101101-tcells.jpg?itok=5jyTRJVG&timestamp=1433965068 1x" media="screen and (min-width: 0)" />
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<img src="https://www.nih.gov/sites/default/files/styles/floated_media_breakpoint-medium/public/news-events/research-matters/2010/20101101-tcells.jpg?itok=eIugob4N&timestamp=1433965068" alt="Microscope image of red, green and blue cells in a mouse spleen" title="Microscope image of red, green and blue cells in a mouse spleen" />
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</picture><span class="caption">Immune cells in the mouse spleen, a site of Th17 development. Helper T cells are in green.</span><span class="credit">Lane and McConnell, courtesy of Wellcome Images. </span></div>
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</div><p>Researchers discovered a new pathway for the development of Th17 cells, a type of helper T cell involved in autoimmunity. The finding reveals potential new targets for treating autoimmune diseases.</p>
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<p>Autoimmune diseases arise when the immune system, which normally protects the body from invading microbes, mistakenly attacks the body’s own tissues. These diseases include type 1 diabetes, psoriasis and multiple sclerosis. The immune system employs many different types of cells to regulate disease. A better understanding of the complex signals between these cells will help researchers design better ways to prevent and treat autoimmune diseases.</p>
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<p>T cells play a major role in the immune system. They can be divided into 2 categories: cytotoxic, which kill infected cells directly, and helper, which make proteins called cytokines that instruct other cells to make certain molecules, move to a specific location or develop in a particular way. Depending on which cytokines are present as a T cell matures, it can become one of many types of helper T cell, each of which has a distinct role in immunity.</p>
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<p>A team led by Dr. John O’Shea of NIH’s National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) set out to investigate the development of Th17 cells. These helper T cells make a cytokine called IL-17 that causes inflammation. While helpful for fighting infections, Th17 cells have also been linked with several autoimmune disorders.</p>
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<p>Past studies have found that a combination of 3 cytokines—interleukin-1-beta (IL-1-beta), interleukin-6 (IL-6) and transforming growth factor beta (TGF-beta)—drive Th17 cell development. However, TGF-beta also drives the development of other T cells (regulatory T cells) that dampen the inflammatory response and help prevent autoimmunity.</p>
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<p>To further explore Th17 development, the scientists exposed immature mouse T cells to a variety of cytokines in culture. As reported in the October 21, 2010, issue of <em>Nature</em>, replacing TGF-beta with another cytokine, IL-23, worked just as well. Gene expression analysis found that Th17 cells from TGF-beta cultures had higher levels of an anti-inflammatory cytokine called IL-10. In contrast, Th17 cells developed with IL-23 showed higher levels of IL-18R1 and T-bet—2 molecules known to be involved in the development of experimental autoimmune encephalomyelitis (EAE), a mouse disease that resembles human multiple sclerosis.</p>
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<p>The researchers next looked at the ability of both sets of Th17 cells to cause autoimmune disease. They transferred the cells into mice engineered to lack mature T cells of their own. Mice that received Th17 cells from IL-23 cultures showed more severe symptoms of EAE. This shows that Th17 cells behave differently depending on which cytokines drove their development, with IL-23 producing Th17 cells that are more likely to cause autoimmune disease.</p>
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<p>These findings shed light on Th17 development, revealing 2 kinds of Th17 cells with distinct functions. The discovery of IL-23 as a driving force in Th17 development points to potential new targets for therapies against autoimmunity.</p>
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</div><h2 class="label-above">Related Links</h2><ul class="spaced print-urls"><li><a href="http://www.niams.nih.gov/Health_Info/Autoimmune/default.asp" target="_top">Autoimmune Disease</a></li><li><a href="https://www.niaid.nih.gov/research/immune-cells" target="_top">Immune Cells</a></li></ul>
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<h3 class="block__title">About NIH Research Matters</h3>
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<p><strong>Editor:</strong> Harrison Wein, Ph.D.</p>
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<p><strong>Assistant Editors:</strong> Vicki Contie and Brian Doctrow, Ph.D.</p>
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<p><strong><em>NIH Research Matters </em></strong>is a weekly update of NIH research highlights reviewed by NIH’s experts. It's published by the <a href="/institutes-nih/nih-office-director/office-communications-public-liaison">Office of Communications and Public Liaison</a> in the <a href="/institutes-nih/nih-office-director">NIH Office of the Director</a>.</p>
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<p>ISSN 2375-9593</p>
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