Article first published online: 6 APR 2010
Copyright © 2010 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 62, Issue 7, page 2182, July 2010
How to Cite
Bilgic, H., Peterson, E. J. and Reed, A. M. (2010), Reply. Arthritis & Rheumatism, 62: 2182. doi: 10.1002/art.27493
- Issue published online: 29 JUN 2010
- Article first published online: 6 APR 2010
To the Editor:
In their letter, Dr. Maddur et al describe their experiments examining potential cellular sources of inflammatory cytokines and chemokines. Their results suggest that under conditions of stimulation with type I IFN, myeloid DCs may produce proinflammatory molecules implicated in the pathogenesis of DM. Maddur and colleagues found that type I IFN significantly enhanced the secretion of IL-8, IL-6, and IL-1β, and moderately enhanced tumor necrosis factor α (TNFα) production by cultured human myeloid DCs in vitro. These results complement our observation of elevated IL-6 levels in DM sera and identify myeloid DCs as a possible cellular source of the enhanced concentrations of IL-6 in DM patients. However, in contrast to the results obtained by Maddur et al, we observed decreased serum IL-8 and TNFα levels in our adult DM cohort. In addition, DM patient sera displayed increased levels of the type I IFN-regulated chemokine CCL3, while in Maddur and colleagues' study the in vitro–derived myeloid DCs did not elaborate this molecule. These data suggest that the regulation of proinflammatory cytokine subsets and type IFN–driven molecules in DM may involve additional cellular mechanisms.
Plasmacytoid DCs constitute one such potential contributing population. Investigators in our group recently reported that muscle biopsy specimens from patients with juvenile DM contained largely plasmacytoid DCs rather than myeloid DCs; these tissue-resident plasmacytoid DCs expressed several proinflammatory chemokines (Lopez de Padilla CM, Vallejo AN, McNallan KT, Vehe R, Smith SA, Dietz AB, et al. Plasmacytoid dendritic cells in inflamed muscle of patients with juvenile dermatomyositis. Arthritis Rheum 2007;56:1658–68). Future in vivo and tissue-based studies will help define the extent to which such cells contribute to type I IFN–driven chemokine production in DM and other autoimmune diseases.
Hatice Bilgic Phd*, Erik J. Peterson MD*, Ann M. Reed MD, * University of Minnesota, Minneapolis, MN, Mayo Clinic, Rochester, MN.