Autoimmune debate resolved?

New findings help resolve a long-standing debate in immunology over what type of cells are behind the progression of type-1 diabetes: attacker or protector cells. Scientists found that linkurl:autoimmune;http://www.the-scientist.com/supplement/2007-5-1/ destruction is likely due to a defect in levels of a cytokine within insulin-producing islets that reduce the numbers of protector cells. The research was published in today's online issue of linkurl:__Immunity.__;http://www.immunity.

By | May 8, 2008

New findings help resolve a long-standing debate in immunology over what type of cells are behind the progression of type-1 diabetes: attacker or protector cells. Scientists found that linkurl:autoimmune;http://www.the-scientist.com/supplement/2007-5-1/ destruction is likely due to a defect in levels of a cytokine within insulin-producing islets that reduce the numbers of protector cells. The research was published in today's online issue of linkurl:__Immunity.__;http://www.immunity.com/content/article/abstract?uid=PIIS1074761308001908 IL-2 is a cytokine that paradoxically affects both the immune cells that protect the insulin producing beta-cells, the T regulatory (Tregs) cells, and the ones that attack them, the T-effector (Teff) cells. Some reports have shown that Treg numbers increased with diabetes onset, while other papers have shown a decrease in Treg numbers. After painstaking quantitative thin-section analysis in NOD mice, a model system for type 1 diabetes, researchers realized that numbers of Tregs were high in some areas and low in others. "You cannot find a defect in these cells [Tregs] anywhere in the body -- except inside the islets," where there was a marked decrease, said Qizhi Tang from University of California, San Francisco, one of the two first authors on the report. Tregs depend on signals, like IL-2 produced by other immune cells, for their survival. However, researchers found abnormally low levels of IL-2 production in the pancreatic islets. When they injected early diabetic mice with low levels of IL-2, the disease progression was halted. "Here they're showing that the reduced IL-2 production is linked to survival of Tregs," said Roland Tisch, a professor of microbiology and immunology at the University of North Carolina at Chapel Hill, who was not involved in the study. Without a sufficient number of healthy Tregs supported by IL-2 in the pancreatic islets, the destruction of the islet cells continues. "You could treat diabetic patients," with this approach, said Tang, but it would be "really critical to determine the right dosing." Given IL-2's dual role -- promoting Treg survival at low levels, but activating destructive Teff proliferation at high levels -- the cytokine could not be used in patients as a stand-alone linkurl:treatment,;http://www.the-scientist.com/article/home/23394/ and would have to include another drug that reduced the chances of activating Teff cells, said Tang.

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