scholarly journals B lymphocyte subpopulations in chronic lymphocytic leukemia

Blood ◽  
1976 ◽  
Vol 47 (2) ◽  
pp. 229-235 ◽  
Author(s):  
RA Rudders

Abstract We have defined two subpopulations of B lymphocytes in chronic lymphocytic leukemia (CLL). The major variant (termed typical) was characterized by the presence of a relatively homogeneous population of small-to-medium-sized lymphocytes with low-density SmIgM and no evidence of intracellular Ig synthesis. A minor group (termed atypical) was identified by the presence of a pleomorphic cell population with few small lymphocytes. The predominant SmIg was IgG, which was detected intracellularly as well as in the serum. The atypical group appeared to be an arrest at a later stage of differentiation where a switch from IgM to IgG synthesis and secretion had occurred. Clinical correlation suggested several clear-cut differences in clinicopathologic characteristics, but the median survivals for both groups at 2 yr was nearly identical.

Blood ◽  
1976 ◽  
Vol 47 (2) ◽  
pp. 229-235
Author(s):  
RA Rudders

We have defined two subpopulations of B lymphocytes in chronic lymphocytic leukemia (CLL). The major variant (termed typical) was characterized by the presence of a relatively homogeneous population of small-to-medium-sized lymphocytes with low-density SmIgM and no evidence of intracellular Ig synthesis. A minor group (termed atypical) was identified by the presence of a pleomorphic cell population with few small lymphocytes. The predominant SmIg was IgG, which was detected intracellularly as well as in the serum. The atypical group appeared to be an arrest at a later stage of differentiation where a switch from IgM to IgG synthesis and secretion had occurred. Clinical correlation suggested several clear-cut differences in clinicopathologic characteristics, but the median survivals for both groups at 2 yr was nearly identical.


Blood ◽  
1978 ◽  
Vol 52 (5) ◽  
pp. 886-895 ◽  
Author(s):  
M Borgers ◽  
H Verhaegen ◽  
M De Brabander ◽  
J De Cree ◽  
W De Cock ◽  
...  

Abstract Purine nucleoside phosphorylase (PNP), the enzyme schematically next to adenosine deaminase in the purine salvage pathway, has been demonstrated cytochemically in peripheral blood lymphocytes of healthy subjects and chronic lymphocytic leukemia (CLL) patients. The enzyme activity is confined to the cytosol. In healthy subjects the majority of lymphocytes are strongly reactive for PNP, whereas the rest are devoid of cytochemically demonstrable activity. The percentage of PNP- positive cells largely corresponds to the number of E rosette-forming cells and is inversely proportional to the number of Ig-bearing cells. In six of seven CLL patients studied only a minor percentage of the lymphocytes showed strong PNP activity, whereas the large majority (88%- -98%) possessed trace activity. Such patients have a high number of Ig- bearing cells and a low number of E rosette-forming cells. A different pattern of markers was found in the lymphocytes of the seventh CLL patient: 66% were strongly reactive for PNP, an important number formed E rosettes, and a minor percentage were Ig bearing. These data indicate that PNP can be useful as a “nonmembrane” marker in the differentiation of the B and T cell origin in CLL and deserves to be studied in other lymphoproliferative disorders.


Blood ◽  
2002 ◽  
Vol 100 (8) ◽  
pp. 2973-2979 ◽  
Author(s):  
Anne J. Novak ◽  
Richard J. Bram ◽  
Neil E. Kay ◽  
Diane F. Jelinek

B-cell chronic lymphocytic leukemia (B-CLL) is defined by the accumulation of CD5+ B cells in the periphery and bone marrow. This disease is not characterized by highly proliferative cells but rather by the presence of leukemic cells with significant resistance to apoptosis and, therefore, prolonged survival. B-lymphocyte stimulator (BLyS) is a newly identified tumor necrosis factor (TNF) family member shown to be critical for maintenance of normal B-cell development and homeostasis and it shares significant homology with another TNF superfamily member, APRIL. The striking effects of BLyS on normal B-cell maintenance and survival raises the possibility that it may be involved in pathogenesis and maintenance of hematologic malignancies, including B-CLL. In this study, we investigated the status of APRIL and BLyS expression, as well as their receptors, in this disease. All B-CLL patient cells studied expressed one or more of 3 known receptors for BLyS; however, the pattern of expression was variable. In addition, we demonstrate for the first time that B-CLL cells from a subset of patients aberrantly express BLyS and APRIL mRNA, whereas these molecules were not detectable in normal B cells. Furthermore, we provide in vitro evidence that BLyS protects B-CLL cells from apoptosis and enhances cell survival. Because these molecules are key regulators of B-cell homeostasis and tumor progression, leukemic cell autocrine expression of BLyS and APRIL may be playing an important role in the pathogenesis of this disease.


2016 ◽  
Vol 5 (5) ◽  
pp. e1132977 ◽  
Author(s):  
Audrey Mohr ◽  
Yves Renaudineau ◽  
Cristina Bagacean ◽  
Jacques-Olivier Pers ◽  
Christophe Jamin ◽  
...  

Blood ◽  
1983 ◽  
Vol 61 (5) ◽  
pp. 940-948 ◽  
Author(s):  
K Itoh ◽  
K Tsuchikawa ◽  
T Awataguchi ◽  
K Shiiba ◽  
K Kumagai

Abstract A case of chronic lymphocytic leukemia that consisted of a homogeneous population of cells that had properties similar to those described for natural killer (NK) cells is presented. These leukemic cells had a morphology of large granular lymphocytes (LGL) and receptors for sheep erythrocytes (ER) and for the Fc portion of IgG (Fc gamma-R). They expressed pan-T antigens OKT3 and Leu-4, but neither helper/inducer T- cell differentiation antigens OKT4 and Leu-3a nor cytotoxic/suppressor T-antigens OKT8 and Leu-2a. HNK 1 antigen, which can be expressed on human NK cells, could be detected on almost all leukemic cells (LGL), whereas a myeloid differentiation antigen, OKM1, which can be expressed on macrophages, granulocytes, and NK cells, was not detected. Thus, it was concluded that the leukemia cells had a characteristic profile of the surface markers: ER+, Fc gamma-R+, HNK-1+, OKT3+, Leu-4+, OKT4-, OKT8-, Leu-3a, Leu-2a, and OKM1-. Although freshly isolated leukemic cells showed no cytotoxicity on NK targets, after incubation at 37 degrees C, the cells did show a potent cytotoxicity on targets of erythroleukemic cell, T cell, and monocyte (but not B cell) origins. When the cells were incubated at 37 degrees C, interferon (IFN gamma) was spontaneously produced in the culture fluids. Treatment with anti- HNK-1 and complement completely abrogated expression of NK activity and interferon production of the patient's lymphocytes in culture. These characteristic features of surface markers and functions strongly suggest the possibility that the leukemia cells of this case are of NK cell origin. The relationship between this case and chronic lymphocytic leukemia of T-cell origin is discussed.


Blood ◽  
1981 ◽  
Vol 57 (2) ◽  
pp. 324-327 ◽  
Author(s):  
P Rambotti ◽  
S Davis

Abstract Lactic dehydrogenase (LDH) was quantitated and the isozyme pattern studied in lymphocyte subpopulations from normal people and patients with chronic lymphocytic leukemia (CLL). Normal T lymphocytes differed from normal B lymphocytes in having greater total LDH activity (597.2 versus 252.1). Total LDH activity in CLL T cells (347.1) was lower than normal T cells., but not significantly different than normal B cells. Total LDH activity in CLL B cells (124.6) was lower then normal B cells and normal T cells. The isozyme pattern of normal T lymphocytes showed a higher activity in the LDH-1 band (26.7% versus 5.4%) but showed a lower activity in LDH-5 band (4.3% versus 16.3%) compared to normal B cells. Chronic lymphocytic leukemia T cells could be distinguished from CLL B cells by a high LDH-5 band (22.3% versus 7.6%) and from normal T cells by a high LDH-5 band (22.3% versus 4.3%) and a low LDH-1 band (7.3% versus 26.7%). CLL B cells could be distinguished from normal B cells by a low LDH-5 band (7.6% versus 16.3%). Thus, the LDH isozyme pattern distinguishes normal T lymphocytes from normal B lymphocytes, and normal T and B lymphocytes from CLL T and B lymphocytes.


Blood ◽  
1988 ◽  
Vol 71 (2) ◽  
pp. 415-421 ◽  
Author(s):  
M Carlsson ◽  
TH Totterman ◽  
P Matsson ◽  
K Nilsson

Abstract The cell cycle transition and differentiation-associated surface antigen expression was studied in a clone of B cell chronic lymphocytic leukemia (B-CLL) with phenotypic properties similar to those of resting B lymphocytes. Differentiation was induced with TPA (12-O-tetradecanoyl- phorbol-13-acetate) and defined and quantitated by morphological and functional markers. Changes in the cell cycle position were determined by flow cytometry of acridine orange-stained cells. The uninduced B-CLL cells represented a homogeneous population with the same cell cycle position (GO) as resting normal peripheral blood lymphocytes. After five days of TPA stimulation, 56% of the B-CLL cells were found in G1A, 9% in G1B, and 3% in the S + G2/M phase, of which 2% was accounted to proliferating T cells. The cell cycle transition of the differentiating B-CLL cells was also examined using cell cycle-associated surface antigens as markers. HLA-DR and CD23 antigens were present already on noninduced cells. The former had a high constant expression, while the amount of CD23 increased upon induction. The 4F2 antigen was absent on noninduced cells but present on 86% of the induced cells. HH1 (CD37) was expressed by the majority of the cells before TPA treatment and decreased to almost undetectable levels within 24 hours. Two antigens related to late stages of the cell cycle, the interleukin 2 (IL 2; CD25) and the transferrin receptor, were present on about 20% of the induced cells. Experiments with enriched T cells showed that T but not B cells incorporated 3H-thymidine. Taken together these results and previous work on the induction of the protooncogene c-myc and c-fos suggest that this B-CLL clone represents GO cells that undergo differentiation without concomitant proliferation when exposed to TPA.


2009 ◽  
Vol 204 (1-6) ◽  
pp. 485-489 ◽  
Author(s):  
Hakan Mellstedt ◽  
Dagny Pettersson ◽  
Göran Holm

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