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Autoimmunity and Transplantation Division, Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Parkville, Victoria, Australia
Aberrant dendritic cell (DC) development and function may
contribute to autoimmune disease susceptibility. To address this
hypothesis at the level of myeloid lineage-derived DC we compared the
development of DC from bone marrow progenitors in vitro and DC
populations in vivo in autoimmune diabetes-prone nonobese diabetic
(NOD) mice, recombinant congenic nonobese diabetes-resistant (NOR)
mice, and unrelated BALB/c and C57BL/6 (BL/6) mice. In
GM-CSF/IL-4-supplemented bone marrow cultures, DC developed in
significantly greater numbers from NOD than from NOR, BALB/c, and BL/6
mice. Likewise, DC developed in greater numbers from sorted
(lineage-IL-7R
-SCA-1-c-kit+)
NOD myeloid progenitors in either GM-CSF/IL-4 or GM-CSF/stem cell
factor (SCF)/TNF-. [3H]TdR incorporation indicated
that the increased generation of NOD DC was due to higher levels of
myeloid progenitor proliferation. Generation of DC with the
early-acting hematopoietic growth factor, flt3 ligand, revealed that
while the increased DC-generative capacity of myeloid-committed
progenitors was restricted to NOD cells, early lineage-uncommitted
progenitors from both NOD and NOR had increased DC-generative capacity
relative to BALB/c and BL/6. Consistent with these findings, NOD and
NOR mice had increased numbers of DC in blood and thymus and NOD had an
increased proportion of the putative myeloid DC
(CD11c+CD11b+) subset within spleen. These
findings demonstrate that diabetes-prone NOD mice exhibit a myeloid
lineage-specific increase in DC generative capacity relative to
diabetes-resistant recombinant congenic NOR mice. We propose that an
imbalance favoring development of DC from myeloid-committed progenitors
predisposes to autoimmune disease in NOD mice.
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