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However, several recent lines of evidence indicated that like most tissues the \u03b2\u2010cell mass is dynamically regulated with ongoing \u03b2\u2010cell regeneration throughout life to replenish lost or damaged \u03b2\u2010cells. In type 1 diabetes (\n                    <jats:styled-content style=\"fixed-case\">T1D<\/jats:styled-content>\n                    ), this fine\u2010tuned balance between \u03b2\u2010cell death and \u03b2\u2010cell renewal in the endocrine pancreas is lost and the deficit in \u03b2\u2010cell mass is largely caused by autoimmune\u2010mediated apoptosis. Currently, the concept that a cure for\n                    <jats:styled-content style=\"fixed-case\">T1D<\/jats:styled-content>\n                    will require both re\u2010establishment of immunological tolerance along with replacement or regeneration of a functional \u03b2\u2010cell mass in\n                    <jats:styled-content style=\"fixed-case\">T1D<\/jats:styled-content>\n                    patients is generally accepted. In this study our current understanding of the events directing \u03b2\u2010cell replication, \u03b2\u2010cell reprogramming from different cell types and \u03b2\u2010cell regeneration is reviewed, in view of the results of various immunomodulatory strategies aiming at blocking autoimmune responses against pancreatic \u03b2\u2010cells and at improving \u03b2\u2010cell mass and function in subjects with\n                    <jats:styled-content style=\"fixed-case\">T1D<\/jats:styled-content>\n                    .\n                  <\/jats:p>","DOI":"10.1111\/dom.12164","type":"journal-article","created":{"date-parts":[[2013,9,4]],"date-time":"2013-09-04T09:27:06Z","timestamp":1378286826000},"page":"98-104","source":"Crossref","is-referenced-by-count":23,"title":["<i>\u03b2<\/i>\n                    \u2010Cell differentiation and regeneration in type 1 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