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Published online before print March 23, 2005
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,1
* Departments of Immunology and
Pulmonary and Critical Care Medicine, Erasmus MC, Rotterdam, The Netherlands
1 Correspondence: Department of Pulmonary and Critical Care Medicine, Erasmus MC, Dr. Molewaterplein 50, 3015GE Rotterdam, The Netherlands. E-mail: t.nikolic{at}erasmusmc.nl
In the nonobese diabetic (NOD) mouse, a model of autoimmune diabetes, dendritic cells (DC), and macrophages (M
) is important for the initiation and progression of autoimmunity and the final destruction of ß-cells. Previous studies suggested that an aberrant development of DC and M is related to their pathogenic function. To study this in vivo, we investigated NOD mouse monocytes, the direct precursors of DC, and M. The recently described discrimination between immature (Ly-6Chigh) and mature (Ly-6Clow) monocytes enabled us to investigate the apportioning between blood monocyte populations in the NOD mouse, which had an abnormally high number of mature monocytes in circulation, and this phenomenon appeared to be intrinsic to the NOD background, as nonobese resistant (NOR) and NOD-H2b mice also showed this altered balance. After depletion by apoptosis-inducing liposomes, the reappearance and transition of immature-to-mature monocytes had similar kinetics as control mice but led again to the presence of a larger, mature monocyte compartment in the blood. In addition, although monocytes from C57BL mice down-regulated their capability to adhere to fibronectin and intercellular adhesion molecule-1 upon maturation, the mature NOD monocytes retained their high adhesion capacity, characteristic of immature cells. Furthermore, both monocyte subpopulations of NOD mice showed enhanced differentiation into M-like F4/80high cells in vitro. In conclusion, mice with the NOD background have raised numbers of mature monocytes in the circulation and a proinflammatory, M-directed monocyte development.
Key Words: autoimmunity • development • antigen-presenting cells • phagocytes
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