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International Immunology, Vol. 14, No. 6, pp. 677-684, June 2002
© 2002 Japanese Society for Immunology

Cell-intrinsic effects of non-MHC NOD genes on dendritic cell generation in vivo

Simon J. Prasad1,2 and Christopher C. Goodnow1

1 Medical Genome Centre, John Curtin School of Medical Research, Australian National University, Canberra, ACT 0200, Australia 2 Present address: Malaghan Institute of Medical Research, PO Box 7060, Wellington South, New Zealand

Correspondence to: C. Goodnow; E-mail: Chris.Goodnow{at}anu.edu.au
Transmitting editor: A. Kelso

Genes outside the MHC create a general susceptibility to autoimmunity in non-obese diabetic (NOD) mice. Here we describe marked differences in dendritic cell generation in vivo, caused by non-MHC NOD genes. Analyses of splenic dendritic cells from the autoimmunity-prone NOD.H-2k mice revealed a relative over-representation of the CD8{alpha}– subsets, in contrast to the level of these subsets observed in the autoimmunity-resistant B10.H-2k congenic strain or other H-2k strains. The imbalance towards CD8{alpha}– dendritic cells was selectively manifested by NOD.H-2k-derived cells in radiation chimeras reconstituted with equal mixtures of NOD.H-2k and B10.H-2k bone marrow cells. In addition to the cell-intrinsic imbalance in dendritic cell subsets, the myeloid lineage overall was intrinsically altered by NOD genes, as this lineage was disproportionately derived from the NOD.H-2k donor in mixed chimeras. These results identify a striking effect of non-MHC NOD genes upon the balance of dendritic cell subsets that may contribute to the generalized defects in self-tolerance in the NOD strain.

Keywords: autoimmune diabetes, dendritic cell subsets, H-2 congenic NOD mice, myeloid precursors, non-MHC NOD genes


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