Journal article

NOD mice are functionally deficient in the capacity of cross-presentation

Chin-Nien Lee, Andrew M Lew, Ken Shortman, Li Wu



Cross-presentation by CD8(+) conventional dendritic cells (cDCs) is involved in the maintenance of peripheral tolerance and this process is termed cross-tolerance. Previous reports showed that non-obese diabetic (NOD) mice have reduced number of splenic CD8(+) cDCs compared with non-diabetic strains, and that the administration of Flt3L to enhance DC development resulted in reduced diabetes incidence. As CD8(+) cDCs are the most efficient antigen cross-presenting cells, it was assumed that reduced cross-presentation by non-activated, tolerogenic CD8(+) cDC predisposes to autoimmune diabetogenesis. Here we show for the first time that indeed NOD mice have a defect in autoantigen cross-present..

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University of Melbourne Researchers


Awarded by National Health and Medical Research Council of Australia (NHMRC)

Awarded by Juvenile Diabetes Research Foundation (JDRF)

Funding Acknowledgements

We thank A. D'Amico, D. Vremec, and J. Pooley for technical assistance. This work was supported by grants from the National Health and Medical Research Council of Australia (NHMRC) (NHMRC Program 1037321), (NHMRC Project 1043414) and Juvenile Diabetes Research Foundation (JDRF) (JDRF 112613), (JDRF 447718) and was made possible through Victorian State Government Operational Infrastructure Support and Australian Government NHMRC IRIIS. CL has been supported by The Melbourne International Research Scholarships (MIRS), the Melbourne International Fee Remission Scholarship (MIFRS) from The University of Melbourne, and the Edith Moffatt funding from The Walter and Eliza Hall Institute of Medical Research.