Chronic lymphocytic leukemia: A proliferative or accumulative disorder?

Dormer, Peter G.; Theml, H; Lau, B.

doi:10.1016/0145-2126(83)90052-8

Cited by 34 publications

(17 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, 51 Cr labeling of CLL cells demonstrated that they leave the circulation less rapidly than normal B lymphocytes, 11 and [ 3 H]thymidinelabeled CLL cells were shown to survive in the circulation of a CLL patient for many weeks without any evidence of extravasation. 10 In line with this, several in vitro studies 12,26,27 have shown that the CLL cell has a reduced capacity to adhere to and/or transmigrate through endothelial-cell monolayers compared with normal B cells, whereas an increased adhesion to endothelium is observed in the more advanced stages. 8,9,27 A recent study 13 has also shown a severely impaired in vitro TEM capacity and in vivo homing of human PB CLL cells to murine peripheral LNs compared with normal B lymphocytes, which has been related to a defective integrin expression by CLL cells.…”

Section: Discussionmentioning

confidence: 75%

“…5,6,8 Finally, several lines of evidence have suggested that CLL cells could have an altered capacity to migrate into the different tissue compartments. [10][11][12][13] Hence, further work is necessary to unravel the mechanisms of CLL-cell extravasation into tissues through the definition of new molecular players. 14 CLL cells differentially express some members of the Eph receptor tyrosine kinase family, partially correlating with clinical features.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

An impaired transendothelial migration potential of chronic lymphocytic leukemia (CLL) cells can be linked to ephrin-A4 expression

Trinidad

Ballesteros

Zuloaga

et al. 2009

Blood

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 75%

Section: Introductionmentioning

confidence: 99%

An impaired transendothelial migration potential of chronic lymphocytic leukemia (CLL) cells can be linked to ephrin-A4 expression

Trinidad

Ballesteros

Zuloaga

et al. 2009

Blood

View full text Add to dashboard Cite

“…These slower kinetics of transmigration of B-CLL cells agrees with in vivo evidence that B-CLL lymphocytes have an impaired capacity to undergo recirculation. Thus, B-CLL lymphocytes labelled by 3 H-thymidine infusion in one patient survived in the circulation for many weeks without evidence of dilution in the far larger extravascular lymphoid tissue (Dormer et al, 1983). Results of studies with B-CLL lymphocytes labelled with 51 chromium also show that these cells leave the circulation less rapidly than lymphocytes from normal subjects (Bazerbashi et al, 1978).…”

Section: Discussionmentioning

confidence: 96%

Transendothelial migration of lymphocytes in chronic lymphocytic leukaemia is impaired and involved down-regulation of both L-selectin and CD23

Chen

Dao

et al. 1999

Br J Haematol

View full text Add to dashboard Cite

Summary.Chronic lymphocytic leukaemia (B-CLL) is characterized by a progressive accumulation of B lymphocytes in blood and bone marrow and high concentrations of soluble CD23 and L-selectin are found in the serum of these patients. In this study lymphocytes from normal subjects and patients with B-CLL were allowed to undergo transendothelial migration across confluent layers of human umbilical vein endothelial cells. Lymphocytes in B-CLL samples showed an impaired capacity to migrate while the minor proportion of normal T cells was enriched by a mean of 2·5-fold in the transmigrated lymphocytes. In contrast, the ratio of B to T lymphocytes in normal preparations was unchanged in the transmigrated population. The expression of adhesion molecules on B-CLL lymphocytes before and after transendothelial migration was studied by flow cytometry which showed that 71 Ϯ 5% of L-selectin was lost from the surface of transmigrated lymphocytes. T and B cells from normal subjects also showed a major loss of L-selectin after transmigration. B-CLL lymphocytes and normal B cells expressed CD23 but this molecule was down-regulated following transendothelial migration, whereas the expression of VLA-4, ICAM-1, LFA-1 and CD44 was unchanged. Lymphocytes incubated with oxidized ATP, an irreversible inhibitor of P2Z/P2X7 purinoceptors, retained their capacity for transendothelial migration and showed the same loss of L-selectin as control leukaemic lymphocytes. Our results show that B-CLL lymphocytes have impaired ability for transendothelial migration compared to normal peripheral blood lymphocytes. Moreover, transendothelial migration involves a universal loss of L-selectin and CD23 from lymphocytes which suggests that the high serum levels of soluble L-selectin and CD23 observed in B-CLL may be generated by shedding during the process of transendothelial migration.

show abstract

“…61 A defective egress of the CLL cell population leading to their retention within tissues has also been proposed but not firmly demonstrated. 58 In such case, it is tentative to speculate…”

Section: The Cll Contextmentioning

confidence: 99%

“…[49][50][51][52] In accordance with our study, 24 several lines of evidence support the notion that CLL cells have an impaired migration into tissues that can be linked to an adhesion deficiency to HEV. [53][54][55][56][57][58] CLL cells form proliferation centers or "pseudofollicles" within the infiltrated lymphoid tissues that can contribute to their survival and/or expansion 59,60 and also to the enlargement of lymph nodes or clinical lymphadenopathy observed in some patients. 61 A defective egress of the CLL cell population leading to their retention within tissues has also been proposed but not firmly demonstrated.…”

Section: The Cll Contextmentioning

confidence: 99%

Eph-ephrin bidirectional signaling comes into the context of lymphocyte transendothelial migration

Trinidad

Zapata

Alonso-Colmenar

2010

Cell Adhesion & Migration

View full text Add to dashboard Cite

A better knowledge of the molecular mechanisms that govern leukocyte trafficking is of major relevance for the clinics. Both normal and pathologic extravasation of lymphocytes are a fine-tuned spatio-temporal event of migratory path-finding, likely regulated by molecular guidance cues underlying cell movements in other systems. We have recently reported that members of the Eph family of receptor tyrosine kinases, namely EphA2 and one of its ligands, ephrin-A4 (EFNA4) can mediate in the traffic of chronic lymphocytic leukemia (CLL) cells and presumably of normal B cells between the blood and the tissues. The importance of EphA2-EFNA4 interactions at the endotheliumlymphocyte interface during TEM could rely on their attractive/repulsive properties. In the present work, we expand on those results by including additional insights and new suggestions for future studies that discuss the relevance of these molecules in overall cell adhesion dynamic events.

show abstract

Chronic lymphocytic leukemia: A proliferative or accumulative disorder?

Cited by 34 publications

References 16 publications

An impaired transendothelial migration potential of chronic lymphocytic leukemia (CLL) cells can be linked to ephrin-A4 expression

An impaired transendothelial migration potential of chronic lymphocytic leukemia (CLL) cells can be linked to ephrin-A4 expression

Transendothelial migration of lymphocytes in chronic lymphocytic leukaemia is impaired and involved down-regulation of both L-selectin and CD23

Eph-ephrin bidirectional signaling comes into the context of lymphocyte transendothelial migration

Contact Info

Product

Resources

About