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The pre\u2010diabetic period was divided into two phases: the early phase (days 88 to 116) during which development of spontaneous diabetes is rare and the late phase (day 123 to 200) during which the incidence of spontaneous diabetes is high. As controls ICR mice of common ancestry were also inoculated. During the early phase diabetes was observed in 4\/10 inoculated, 0\/13 control NOD and 7\/13 inoculated ICR males <jats:italic>vs.<\/jats:italic> 6\/12 inoculated, 1\/11 control NOD and 0\/15 inoculated ICR females. However, in NOD female, virus\u2010induced diabetes prevalence was variable from one experiment to another. In parallel the flow cytometric analysis showed a high percentage of L3T4<jats:sup>+<\/jats:sup> T lymphocytes in the pancreas of inoculated female NOD mice 10 days after the infection. At this time a large proportion of both L3T4<jats:sup>+<\/jats:sup> and Ly\u20102<jats:sup>+<\/jats:sup> cells expressed the interleukin 2 receptor. During the late phase no new case of diabetes occurred in inoculated NOD mice but one case was observed in control NOD males and five in control NOD females. This prevention of autoimmune diabetes was constantly found in other experiments. Insulitis was milder in inoculated NOD mice of both sexes than in control NOD. Adoptive transfer of diabetes into irradiated 8\u2010week\u2010old males by splenocytes from 28\u2010week\u2010old females was successful in five out seven attempts with control splenocytes and in zero out of six attempts with splenocytes from inoculated mice. This immunosuppression was specific as the ability of lymphocytes to respond to soluble or allogeneic antigens was preserved.<\/jats:p><jats:p>In the early phase EMCV\u2010D precipitated the onset of diabetes in females NOD mice by amplifying L3T4<jats:sup>+<\/jats:sup> T lymphocyte\u2010mediated immune mechanisms. During the late phase viral infection had lessened immune processes in animals which had resistedor recovered from virus\u2010induced diabetes.<\/jats:p>","DOI":"10.1002\/eji.1830200615","type":"journal-article","created":{"date-parts":[[2007,3,1]],"date-time":"2007-03-01T12:08:28Z","timestamp":1172750908000},"page":"1297-1303","source":"Crossref","is-referenced-by-count":39,"title":["Paradoxical lessening of autoimmune processes in non\u2010obese diabetic mice afterinfection with the diabetogenic variant of encephalomyocarditis virus"],"prefix":"10.1002","volume":"20","author":[{"given":"Laurence","family":"Hermitte","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bernard","family":"Vialettes","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philippe","family":"Naquet","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Catherine","family":"Atlan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marie\u2010jos\u00e9","family":"Payan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philippe","family":"Vague","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2005,11,17]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.2337\/diabetes.37.3.257"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1538\/expanim1978.29.1_1"},{"key":"e_1_2_1_4_2","first-page":"285","volume-title":"Clinico\u2010Genetic Genesis of Diabetes mellitus","author":"Mimura G.","year":"1982"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.165.6.1639"},{"key":"e_1_2_1_6_2","doi-asserted-by":"crossref","first-page":"855","DOI":"10.2337\/diab.35.8.855","volume":"35","author":"Wicker L. 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