机译：转基因诱导的GAD耐受性限制了早期β-细胞自身反应性的发展，但导致随后对其他β-细胞抗原的超常自身反应性的发展。
Jide Tian,1 Hoa Dang,1 Harald von Boehmer,2 Elmar Jaeckel,3 and Daniel L. Kaufman1From the 1 Department of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, the 2 Laboratory of Lymphocyte Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts, and the 3 Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.Corresponding author: Daniel L. Kaufman, dkaufman@mednetucla.edu.Received 25 June 2008 and accepted 1 September 2009. Published ahead of print at http://diabetes.diabetesjournals.org on 9 September 2009. DOI: 10.2337/db08-0851.© 2009 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommorLS.org/Ucenaes/by -nc-nd/3.0/ for details.The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.,;
机译：转基因诱导的GAD耐受性限制了早期β细胞自身反应性的发展，但导致随后超常自身反应性发展为其他β细胞抗原的发展。
机译：LF 15-0195通过诱导自身反应性CD4 T细胞的长期耐受来抑制大鼠中枢神经系统自身免疫的发展
机译：LF 15-0195通过诱导自身反应性CD4 T细胞的长期耐受来抑制大鼠中枢神经系统自身免疫的发展
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机译：在正常和自身免疫遗传背景下B细胞发育过程中RNA特异性自身反应性B细胞的活化
机译：转基因诱导的GAD耐受性限制了早期β细胞自身反应性的发展但导致随后超常自身反应性发展为其他β细胞抗原的发展。
机译：转基因诱导的GAD耐受性限制了早期β细胞自身反应性的发展，但导致随后超常自身反应性发展为其他β细胞抗原的发展。
