{"id":4831,"date":"2016-04-13T00:00:00","date_gmt":"2016-04-13T06:00:00","guid":{"rendered":"https:\/\/www.uchealth.org\/today\/2016\/04\/13\/cu-researchers-key-to-diabetes-may-be-in-the-hips\/"},"modified":"2023-04-21T13:54:03","modified_gmt":"2023-04-21T19:54:03","slug":"cu-researchers-key-to-diabetes-may-be-in-the-hips","status":"publish","type":"post","link":"https:\/\/www.uchealth.org\/today\/cu-researchers-key-to-diabetes-may-be-in-the-hips\/","title":{"rendered":"CU researchers: key to diabetes may be in the HIPs"},"content":{"rendered":"
<\/div>

Decades of painstaking laboratory work has led a University of Colorado School of Medicine team to a fundamental discovery pointing to the roots of Type 1 diabetes and, possibly, other autoimmune diseases. They identified what appears to be the molecular lure that leads T cells \u2013 which normally protect the body from invaders \u2013 to mistakenly attack and destroy the pancreas\u2019s insulin-producing cells. The result: 1.25 million people<\/a> in the United States who must rely on insulin pumps or injections for the rest of their lives.<\/p>\n

Thomas Delong, PhD, and Kathryn Haskins, PhD<\/a>, led a CU Department of Immunology & Microbiology team in the effort, the results of which were recently published<\/a> in the prestigious journal Science<\/em>.<\/p>\n

Delong, a biochemist and himself a Type 1 diabetic, arrived at CU from the University of Erlangen-Nuremberg in Germany a decade ago. He came to apply his expertise in chemistry to an effort Haskins had started in the late 1980s to study T cell clones from mice that spontaneously develop autoimmune diabetes. The aim all along was to find out what antigen or antigens in the pancreas\u2019s insulin-producing beta cells were activating T cells and triggering the autoimmune attack that leads to Type 1 diabetes.<\/p>\n

Understanding that trigger would give researchers an invaluable tool for developing new ways of testing for Type 1 diabetes long before symptoms appear and creating therapies to stop the disease\u2019s progression before the body\u2019s own immune system wipes out the pancreas\u2019s ability to produce insulin.<\/p>\n

Tough problem<\/strong><\/p>\n

\"Thomas
Thomas Delong and Katie Haskins in their lab in the Barbara Davis Center for Childhood Diabetes.<\/figcaption><\/figure>\n

When Delong arrived in 2006, it was thought that the antigens that attracted T cells were proteins neatly encoded by some straightforward section of DNA. The most obvious of these would have been insulin itself, which, given Type 1 diabetes\u2019 attack on insulin-producing cells, might logically play the role of blood in shark-infested waters.<\/p>\n

It\u2019s a neat comparison that unfortunately isn\u2019t quite so pat. \u201cThis is a very difficult problem,\u201d Haskins said. \u201cT cells don\u2019t respond to a protein as a whole protein \u2013 that protein has to be broken up into pieces.\u201d<\/p>\n

Cells routinely break apart, reconstitute, tweak and customize proteins as they roll off their molecular assembly lines in a process called post-translational modification, Haskins explained. She and Delong hypothesized that whatever rogue antigen was attracting T cells in the pancreas was probably a function of the protein modification process going awry without leaving an obvious blueprint behind.<\/p>\n

\u201cIt\u2019s a black box,\u201d Delong said. \u201cYou don\u2019t know what the T cell is actually seeing.\u201d<\/p>\n

Pep rally<\/strong><\/p>\n

And so Delong focused on chunks of proteins called peptides. He synthesized them, purified them, and tested how attractive they were to a panel of lab-grown mouse T cell clones. By 2010, he had found T cells to be weakly attracted to a peptide called WE14, a short chain of amino acids lopped off a protein called chromogranin A that is abundant in beta cells produced by the pancreas.<\/p>\n

Delong wasn\u2019t especially excited. \u201cThe T cells responded poorly \u2013 it was a lousy antigen,\u201d he said.<\/p>\n

But at least T cells did respond. The discovery of something even remotely magnetic to rogue pancreatic T cells was enough to land the work<\/a> in Nature Immunology<\/em>. Delong and Haskins then focused on possible combinations of peptides that pancreas cells might put together, Lego-like, through post-translational modification.<\/p>\n

\u201cWe were looking for the needle in the haystack,\u201d Delong said. But it was really nothing so simple as that, he added. With WE14, \u201cWe knew a piece of the needle, but we suspected the needle was somewhat modified. It was painted like hay.\u201d<\/p>\n

Trial and error<\/strong><\/p>\n

Delong proceeded to invent different combinations of peptides that might combine with WE14. The idea was to create an antigen that pancreas cells could conceivably be synthesizing that attracted T cell friendly fire. He called them hybrid insulin peptides, or HIPs, and the library of 187 of them he created itself broke new ground in the field of immunology, Haskins says. Delong tested many combinations with cloned mouse T cells, waited 24 hours, and looked for gamma interferon, an inflammatory protein that T cells release when the right antigen whets their appetite for destruction.<\/p>\n

Insulin, it turned out, did play a role in that \u2013 but in the form of a fragment of a peptide cleaved from insulin cells. The fragment chemically bonded with the WE14 amino acid chain, and the resulting HIP lit up the T cells.<\/p>\n

Delong then worked backwards, using mass spectrometry to characterize the chemical architecture of his creation and confirming that it indeed occurs in mouse cells. With collaborators in Massachusetts and Australia, he found that HIPs could also be targets for human T cells isolated from the pancreases of deceased donors with Type 1 diabetes. Ten years of work and many hundreds of thousands of dollars from the National Institutes of Health, the American Diabetes Association, and the Juvenile Diabetes Research Foundation had led to what Haskins described as \u201ca game-changer.\u201d<\/p>\n

Toward a cure<\/strong><\/p>\n

\"Timothy
Timothy Wiles, a PhD student who, like Delong, has Type 1 diabetes, at work in the lab.<\/figcaption><\/figure>\n

Delong, Haskins and colleagues are now working on developing therapies based on the HIP antigen that can turn off Type 1 diabetes in mice and, if it works, humans. With the help of the CU Technology Transfer Office, they filed a patent covering diagnostics and therapeutics based on HIPs on March 4, Haskins said.<\/p>\n

But the work on Type 1 diabetes may be only the beginning. \u201cThis is a whole new type of antigen that could be related to other autoimmune diseases,\u201d Delong said.<\/p>\n

The team is particularly interested in whether hybrid peptides could be antigens in autoimmune thyroiditis, rheumatoid arthritis, multiple sclerosis, and Sjogren\u2019s syndrome, he said. If you know the trigger, you can develop diagnostics to detect disease-driving T cells and, they hope, create therapeutics to prevent full-blown autoimmune disease from developing \u2013 for example, by using other hybrid peptides to re-educate T cells so they lay off the insulin-producing pancreatic beta cells.<\/p>\n

The beauty of such antigen-specific therapy is its narrow targeting \u2013 potentially another application of personalized medicine, Haskins said. You take out only the T cells that are causing the problem, and not helpful T cells, too, as is the case with broad-spectrum immunosuppressants.<\/p>\n

For Delong, his own diabetes played the role of antigen, attracting him to the field he\u2019s now disrupted like a T cell, though in his case in a strictly positive sense.<\/p>\n

\u201cI probably would not be doing diabetes research if I didn\u2019t have it,\u201d he said. \u201cBut that doesn\u2019t change anything about how much I enjoy doing diabetes research.\u201d<\/p>\n","protected":false},"excerpt":{"rendered":"

Decades of painstaking laboratory work has led a University of Colorado School of Medicine team to a fundamental discovery pointing to the roots of Type 1 diabetes and, possibly, other autoimmune diseases. They identified what appears to be the molecular lure that leads T cells \u2013 which normally protect the body from invaders \u2013 to […]<\/p>\n","protected":false},"author":23,"featured_media":2494,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"_relevanssi_hide_post":"","_relevanssi_hide_content":"","_relevanssi_pin_for_all":"","_relevanssi_pin_keywords":"","_relevanssi_unpin_keywords":"","_relevanssi_related_keywords":"","_relevanssi_related_include_ids":"","_relevanssi_related_exclude_ids":"","_relevanssi_related_no_append":"","_relevanssi_related_not_related":"","_relevanssi_related_posts":"","_relevanssi_noindex_reason":"","footnotes":""},"categories":[5],"tags":[981,988,199,200,1046],"class_list":["post-4831","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-innovative-care","tag-barbara-davis-center-for-childhood-diabetes","tag-diabetes-endocrinology-care","tag-diabetes-care","tag-diabetes-prevention","tag-health-screening"],"acf":[],"yoast_head":"\nCU researchers: key to diabetes may be in the HIPs - 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