Circulating blood dendritic cells from myeloid leukemia patients display quantitative and cytogenetic abnormalities as well as functional impairment

Citation
M. Mohty et al., Circulating blood dendritic cells from myeloid leukemia patients display quantitative and cytogenetic abnormalities as well as functional impairment, BLOOD, 98(13), 2001, pp. 3750-3756
Citations number
41
Categorie Soggetti
Hematology,"Cardiovascular & Hematology Research
Journal title
BLOOD
ISSN journal
00064971 → ACNP
Volume
98
Issue
13
Year of publication
2001
Pages
3750 - 3756
Database
ISI
SICI code
0006-4971(200112)98:13<3750:CBDCFM>2.0.ZU;2-Z
Abstract
Dendritic cells (DCs) are responsible for the initiation of immune response s. Two distinct subsets of blood DCs have been characterized thus far. Myel oid DCs (MDCs) and plasmacytoid monocytes (PDCs) were shown to be able to p romote polarization of naive T cells. This study shows a dramatic quantitat ive imbalance in both circulating blood DC subsets in 37 patients with acut e myeloid leukemias. Eleven patients (30%) displayed a normal quantitative profile (MDC mean, 0.37% +/- 0.21%; range, 0.01% to 0.78%; PDC mean, 0.21% +/- 0.24%; range, 0.04% to 0.62%), whereas 22 (59%) showed a tremendous exp ansion of MDCs (9 patients: mean, 16.76% +/- 14.03%; range, 1.36% to 41%), PDCs (4 patients: mean, 7.28% +/- 6.84%; range, 1% to 14%), or both subsets (9 patients: MDC mean, 10.86% +/- 12.36%; range, 1.02% to 37.1%; PDC mean, 4.25% +/- 3.78%; range, 1.14% to 13.04%). Finally, in 4 patients (11%), no DC subsets were detectable. Both MDC and PDC subsets exhibited the origina l leukemic chromosomal abnormality. Ex vivo, leukemic PDCs, but not leukemi c MDCs, had Impaired capacity for maturation and decreased allostimulatory, activity. Also, leukemic PDCs were altered in their ability to secrete int erferon-alpha. These data provide evidence that DC subsets in vivo may be a ffected by leukemogenesis and may contribute to leukemia escape from Immune control. (C) 2001 by The American Society of Hematology.