Hauben, E.Roncarolo, M.Nevo, U.Schwartz, M.2014-03-202014-03-202005Trends in Immunology, 2005; 26(5):248-2531471-49061471-4981http://hdl.handle.net/2440/82240The trigger that leads to the pathogenesis of type 1 diabetes is currently unknown. It is well established that the pathophysiology of the disease is biphasic. In the first stage, leukocytes infiltrate the pancreatic islets in a response that does not cause damage. In the second phase, which occurs only in diabetes-prone individuals and strains, autoreactive T cells acquire aggressive potential and destroy the majority of the pancreatic islets. Rodents and humans exhibit a physiological ripple of apoptotic beta-cell death shortly after birth, which induces an adaptive autoimmune response towards islet-antigens, both in diabetes-prone non-obese diabetic (NOD) mice and in mice that do not develop diabetes. Here, we propose that the early T cell-mediated autoimmune response towards islet-antigens is physiological, purposeful and beneficial.en© 2005 Elsevier Ltd. All rights reserved.B-LymphocytesT-Lymphocyte SubsetsAnimalsHumansDiabetes Mellitus, Type 1ApoptosisCell DifferentiationAutoimmunityImmune ToleranceHomeostasisJournal article002011467410.1016/j.it.2005.03.0040002292499000052-s2.0-2764453537126844Hauben, E. [0000-0002-6062-411X]