![\"MSE](\"\/eng\/files\/2019\/08\/h_research_Vegas-Profile-Pic-1-636x425.jpg\")
Type 1 diabetes is rare but devastating. A person\u2019s own immune system attacks the pancreas, destroying insulin-producing tissue and the body\u2019s ability to regulate blood sugar. About five percent of people with diabetes\u2014approximately 1.25 million Americans\u2014have this form of the disease, according to the American Diabetes Association<\/a>. Unregulated blood sugar can lead to blindness, kidney failure, and death.<\/p>\n Scientists aren\u2019t sure what causes type 1 diabetes, though they suspect that a genetic predisposition, combined with an environmental trigger, causes a sudden disruption in the immune system that causes it to attack the body\u2019s own tissue. The only treatment is a lifetime of careful blood sugar monitoring, with insulin injections as needed.<\/p>\n But what if there were a way to block the immune system before the damage was done, preserving at least some of the pancreas\u2019 ability to produce insulin? That\u2019s the goal of Arturo Vegas<\/a>, a Boston University College of Arts & Sciences assistant professor of chemistry, whose lab combines biology, chemistry, materials science, and engineering to develop targeted therapies for complex diseases like diabetes. He recently was awarded a $2 million Type 1 Diabetes Pathfinder Award from the National Institutes of Health<\/a> (NIH) to pursue the work.<\/p>\n \u201cMost of the therapies today deal with the disease after it\u2019s already there,\u201d says Vegas, a Peter Paul Career Development Professor<\/a>. \u201cWe want to preserve the patient\u2019s own tissue as much as we can. How do we develop technologies that intervene before<\/em> they\u2019ve lost all of their insulin-producing tissue?<\/p>\n \u201cThere\u2019s this very broad range of time when the disease manifests itself,\u201d adds Vegas. \u201cIt actually takes time, and it varies from patient to patient.\u201d<\/p>\n Vegas is going to take advantage of this window and create novel therapies that will either suppress rogue immune cells or strengthen the pancreas\u2019 defenses against them.<\/p>\n \u201cType 1 diabetes is a huge clinical problem, and this is a smart and clever way to approach it,\u201d says Mark Grinstaff<\/a>, a BU professor of chemistry and biomedical engineering.<\/p>\n The defensive position, which Vegas calls \u201ctargeted immunosuppression,\u201d would take existing drugs used to prevent the body\u2019s rejection of organ transplants and tweak them to target specific immune cells.<\/p>\n \u201cWe know the immunosuppressants work. They\u2019re just applied in a way that kind of carpet bombs the body,\u201d says Vegas. \u201cWhat if we can make those drugs a little smarter, and give them a guidance system, so that they\u2019re only going to affect the immune cells that are performing that horrible autoimmune function at the site of the insulin-producing tissue?\u201d<\/p>\n Vegas\u2019 \u201cguidance system\u201d consists of small molecules that are attached to the immunosuppressive drugs and also recognize and attach to cell surface receptors that are unique to insulin-producing tissue. \u201cThe drug goes to that space and then remains there so that when the immune cells come to destroy the insulin-producing tissue, the drug can block the immune cells that are trying to do harm,\u201d he says.<\/p>\n Vegas\u2019 other idea is to go on the offense, designing a molecule that seeks out and destroys rogue immune cells before they get anywhere near the pancreas.<\/p>\n \u201cNormally when our immune system gets matured and educated, the bad-actor cells that might target our own tissue are filtered out,\u201d says Vegas. But in type 1 diabetes, the filtering mechanism is broken and leaks out immune cells specifically designed to attack the insulin-producing tissue. Fortunately, these bad cells have a bulls-eye: a protein marking them as pancreas-attackers. Vegas wants to build a molecule that can bind to this protein and either destroy the immune cell or block its action. \u201cIf you take out these cells, it\u2019s likely that you won\u2019t harm the rest of the immune system,\u201d says Vegas. \u201cYou\u2019re just removing the bad actors.\u201d<\/p>\n Vegas says that his background in biology and chemistry, combined with advanced training in chemical and biomedical engineering in the labs of Robert Langer<\/a> and Daniel Anderson<\/a> at the Massachusetts Institute of Technology, allows him to study problems from several different angles and see patterns and solutions that may have been overlooked.<\/p>\n \u201cArturo\u2019s training positions him to ask really difficult questions that can only be addressed by bringing together several fields, and this NIH funding will enable him to perform the critical experiments to test his hypotheses,\u201d says Grinstaff.<\/p>\n Though Vegas is doing basic research, his ultimate goal is to see his work delivered to patients.<\/p>\n \u201cIf, at the end of my career, I can say, \u2018I developed a technology that was behind that drug,\u2019\u201d he says, \u201cthen I will say I\u2019ve had a very fruitful, accomplished career.\u201d<\/p>\n","protected":false},"excerpt":{"rendered":" Chemist and Material Scientist Arturo Vegas receives $2 million NIH grant to develop therapies that intervene at early stage of Type 1 diabetes. <\/p>\n","protected":false},"author":8588,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[236,909,245],"tags":[],"_links":{"self":[{"href":"https:\/\/www.bu.edu\/eng\/wp-json\/wp\/v2\/posts\/88144"}],"collection":[{"href":"https:\/\/www.bu.edu\/eng\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.bu.edu\/eng\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.bu.edu\/eng\/wp-json\/wp\/v2\/users\/8588"}],"replies":[{"embeddable":true,"href":"https:\/\/www.bu.edu\/eng\/wp-json\/wp\/v2\/comments?post=88144"}],"version-history":[{"count":1,"href":"https:\/\/www.bu.edu\/eng\/wp-json\/wp\/v2\/posts\/88144\/revisions"}],"predecessor-version":[{"id":131342,"href":"https:\/\/www.bu.edu\/eng\/wp-json\/wp\/v2\/posts\/88144\/revisions\/131342"}],"wp:attachment":[{"href":"https:\/\/www.bu.edu\/eng\/wp-json\/wp\/v2\/media?parent=88144"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.bu.edu\/eng\/wp-json\/wp\/v2\/categories?post=88144"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.bu.edu\/eng\/wp-json\/wp\/v2\/tags?post=88144"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}![\"MSE](\"\/eng\/files\/2019\/08\/Beta-cells_400x400.jpg\")