Impaired Peripheral Blood Dendritic Cell Counts in B-Chronic Lymphocytic Leukaemia

Konference: 2006 48th ASH Annual Meeting - účast ČR

Kategorie: Maligní lymfomy a leukémie

Téma: Publikace ve sborníku

Číslo abstraktu: 4966

Autoři: MUDr. Rudolf Horváth, Ph.D.; Vit Budinsky; MUDr. Robert Pytlík, Ph.D.; prof. MUDr. Pavel Klener, DrSc.; Prof. MUDr. Marek Trněný, CSc.; Prof. MUDr. Radek Špíšek, Ph.D.; Prof. MUDr. Jiřina Bartůňková, DrSc.

B-cell chronic lymphocytic leukaemia (B-CLL) is the most common leukaemia of adults in Western worls accounting for about 40% of leukemias in adults over the age of 65 years. Although, B-CLL cells can, under certain conditions, act as antigen presenting cell (APCs) they fail to generate an efficient anti-leukemic immune response. Dendritic cells (DCs) represent the most potent APCs and they are the only cell type capable of initiating a primary immune response. To asses a potential role of DCs compartment in insufficient anti-leukemic and anti-infectious immunity in B-CLL, we have analysed peripheral blood DCs subsets in 17 patients with an early stage B-CLL and 8 age matched controls by multi colour flow cytometry. Dendritic cells were identified by lack of B, T, NK and monocyte markers, HLA-DR expression and expression of CD11c and CD123 for myeloid and plasmacytoid DCs, respectively. We found a significant reduction of absolute plasmacytoid DCs counts in patients with B-CLL (average count = 49,4x106/L) when compared to healthy donors (average count = 111,3 x106/L, p<0,05). Myeloid DCs counts were not different from healthy controls (average count = 192,7x106/L vs. 196,7x106/L p=NS). Number of plasmacytoid DCs decreased with B-CLL cells number. DC counts did not depend on CD38 or ZAP70 expression or immunoglobulin mutational status. Phenotypic analysis of circulating plasmacytoid and myeloid DCs showed low co-stimulation profile comparing to isotype controls. Thus, the depletion of pDCs in B-CLL could represent a mechanism contributing to the poor anti-leukemic immune responses in B-CLL and/or to immune deficiency in CLL patients.
Acknowledgments: This study was supported by projects MSM 0021620808 and MSM 0021620812 from the Ministry of Education, Czech Republic and grant GAUK 52/2004 provided by the internal grant agency of Charles University to RH.

Datum přednesení příspěvku: 9. 12. 2006