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Previous reports showed that non\u2010obese diabetic (NOD) mice have reduced number of splenic CD8<jats:sup>+<\/jats:sup> cDCs compared with non\u2010diabetic strains, and that the administration of Flt3L to enhance DC development resulted in reduced diabetes incidence. As CD8<jats:sup>+<\/jats:sup> cDCs are the most efficient antigen cross\u2010presenting cells, it was assumed that reduced cross\u2010presentation by non\u2010activated, tolerogenic CD8<jats:sup>+<\/jats:sup> cDC predisposes to autoimmune diabetogenesis. Here we show for the first time that indeed NOD mice have a defect in autoantigen cross\u2010presentation capacity. First, we showed that NOD CD8<jats:sup>+<\/jats:sup> cDCs were less sensitive to iatrogenic cytochrome c, which had previously been shown to selectively deplete CD8<jats:sup>+<\/jats:sup> cDCs that functionally cross\u2010present. Second, we found that proliferation of islet\u2010specific glucose\u20106\u2010phosphatase catalytic subunit\u2010related protein (IGRP)\u2010specific CD8<jats:sup>+<\/jats:sup> T cells was impaired in NOD compared with non\u2010obese diabetes resistant mice after immunization with cell associated recombinant fusion protein containing the cognate IGRP peptide. This study, therefore, suggests that the reduced number of CD8<jats:sup>+<\/jats:sup> cDCs in NOD mice, coupled with the reduced capacity to cross\u2010present self\u2010antigens, reduces the overall capacity to maintain peripheral tolerance in the spontaneous autoimmune type 1 diabetes mice.<\/jats:p>","DOI":"10.1038\/icb.2014.119","type":"journal-article","created":{"date-parts":[[2015,1,20]],"date-time":"2015-01-20T10:35:50Z","timestamp":1421750150000},"page":"548-557","source":"Crossref","is-referenced-by-count":10,"title":["NOD mice are functionally deficient in the capacity of cross\u2010presentation"],"prefix":"10.1111","volume":"93","author":[{"given":"Chin\u2010Nien","family":"Lee","sequence":"first","affiliation":[{"name":"Molecular Immunology Division  Parkville VIC Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew M","family":"Lew","sequence":"additional","affiliation":[{"name":"Immunology Division of The Walter and Eliza Hall Institute of 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