The Expression of a Human B-Lymphocyte Antigen and Surface Membrane Immunoglobulin by Lymphoid cells from Patients with Lymphocytic Lymphoma, Multiple Myeloma and Benign Monoclonal Gammapathy

Leukemic cells from 20 patients with chronic lymphocytic leukemia (CLL) and 60 patients with acute lymphocytic leukemia (ALL) were studied for T- and B-lymphocyte cell surface membrane markers. B-cell markers included surface membrane immunoglobulin, erythrocyte-antibody complement rosette formation, and B-cell (a-like or HLA-DR) antigens detected by a B-cell antiserum. T-cell markers included spontaneous sheep red blood cell rosette formation and a cytotoxic reaction to a specific T-cell antiserum. Seven patients with CLL and two with ALL had dual B and T markers. We propose that dual B- and T-cell markers are more common in CLL and ALL patients than previously reported. With newer and more sensitive tests for identification of B and T cells, this observation may be recognized more frequently.

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Dual B and T markers in acute and chronic lymphocytic leukemia

Blood ◽

10.1182/blood.v55.1.16.16 ◽

1980 ◽

Vol 55 (1) ◽

pp. 16-20 ◽

Cited By ~ 44

Author(s):

KA Foon ◽

RJ Billing ◽

PI Terasaki

Keyword(s):

T Cell ◽

Chronic Lymphocytic Leukemia ◽

B Cell ◽

B Lymphocyte ◽

Surface Membrane ◽

Lymphocytic Leukemia ◽

Rosette Formation ◽

Leukemic Cells ◽

Cell Markers ◽

Membrane Immunoglobulin

Abstract Leukemic cells from 20 patients with chronic lymphocytic leukemia (CLL) and 60 patients with acute lymphocytic leukemia (ALL) were studied for T- and B-lymphocyte cell surface membrane markers. B-cell markers included surface membrane immunoglobulin, erythrocyte-antibody complement rosette formation, and B-cell (a-like or HLA-DR) antigens detected by a B-cell antiserum. T-cell markers included spontaneous sheep red blood cell rosette formation and a cytotoxic reaction to a specific T-cell antiserum. Seven patients with CLL and two with ALL had dual B and T markers. We propose that dual B- and T-cell markers are more common in CLL and ALL patients than previously reported. With newer and more sensitive tests for identification of B and T cells, this observation may be recognized more frequently.

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Distribution of carboxypeptidase M on lymphoid and myeloid cells parallels the other zinc-dependent proteases CD10 and CD13

Blood ◽

10.1182/blood.v86.3.1098.1098 ◽

1995 ◽

Vol 86 (3) ◽

pp. 1098-1105 ◽

Cited By ~ 25

Author(s):

B de Saint-Vis ◽

L Cupillard ◽

D Pandrau-Garcia ◽

S Ho ◽

N Renard ◽

...

Keyword(s):

B Lymphocyte ◽

Lymphoblastic Leukemia ◽

Surface Membrane ◽

Leukemia Cell ◽

Myeloid Cells ◽

Peptide Hormones ◽

Lymphoid Cells ◽

Leukemia Cell Line ◽

Expression Cloning ◽

Carboxypeptidase M

Abstract Monoclonal antibody (MoAb) M27 was generated after immunization of mice with the human B-lineage acute lymphoblastic leukemia cell line Pre- ALP. Under reducing conditions, MoAb M27 precipitated a 60-kD surface- membrane molecule from Pre-ALP cells. Expression cloning of Pre-ALP cDNA showed that M27 recognizes carboxypeptidase M (CPM), a cell- surface, zinc-dependent protease known to cleave off basic C-terminal amino acids from peptide hormones. Using M27 antibody, CPM was detected only at discrete B lymphocyte developmental stages, namely on committed precursors and on germinal center cells. CPM was also expressed on mature T cells, mainly after activation. These results provide the first description of a carboxy-peptidase on lymphoid cells. In addition, CPM was found on granulocytes and monocytes, but not on their progenitors. Strikingly, CPM was present only on CD38+ cells, irrespective of lineage affiliation. Of interest, CPM displayed a largely overlapping distribution with the CD10 and CD13 peptidases, with which it shares common substrates (enkephalins, bradykinin). Collectively, the present data show a previously unrecognized distribution pattern of CPM on lymphoid and myeloid cells and suggest that CPM may cooperate with CD10 and CD13 to regulate biologic activity of peptide hormones on leukocytes.

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Distribution of carboxypeptidase M on lymphoid and myeloid cells parallels the other zinc-dependent proteases CD10 and CD13

Blood ◽

10.1182/blood.v86.3.1098.bloodjournal8631098 ◽

1995 ◽

Vol 86 (3) ◽

pp. 1098-1105 ◽

Cited By ~ 1

Author(s):

B de Saint-Vis ◽

L Cupillard ◽

D Pandrau-Garcia ◽

S Ho ◽

N Renard ◽

...

Keyword(s):

B Lymphocyte ◽

Lymphoblastic Leukemia ◽

Surface Membrane ◽

Leukemia Cell ◽

Myeloid Cells ◽

Peptide Hormones ◽

Lymphoid Cells ◽

Leukemia Cell Line ◽

Expression Cloning ◽

Carboxypeptidase M

Monoclonal antibody (MoAb) M27 was generated after immunization of mice with the human B-lineage acute lymphoblastic leukemia cell line Pre- ALP. Under reducing conditions, MoAb M27 precipitated a 60-kD surface- membrane molecule from Pre-ALP cells. Expression cloning of Pre-ALP cDNA showed that M27 recognizes carboxypeptidase M (CPM), a cell- surface, zinc-dependent protease known to cleave off basic C-terminal amino acids from peptide hormones. Using M27 antibody, CPM was detected only at discrete B lymphocyte developmental stages, namely on committed precursors and on germinal center cells. CPM was also expressed on mature T cells, mainly after activation. These results provide the first description of a carboxy-peptidase on lymphoid cells. In addition, CPM was found on granulocytes and monocytes, but not on their progenitors. Strikingly, CPM was present only on CD38+ cells, irrespective of lineage affiliation. Of interest, CPM displayed a largely overlapping distribution with the CD10 and CD13 peptidases, with which it shares common substrates (enkephalins, bradykinin). Collectively, the present data show a previously unrecognized distribution pattern of CPM on lymphoid and myeloid cells and suggest that CPM may cooperate with CD10 and CD13 to regulate biologic activity of peptide hormones on leukocytes.

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Growth of B-lymphocyte colonies in vitro.

Journal of Experimental Medicine ◽

10.1084/jem.142.6.1534 ◽

1975 ◽

Vol 142 (6) ◽

pp. 1534-1549 ◽

Cited By ~ 103

Author(s):

D Metcalf ◽

G J Nossal ◽

N L Warner ◽

J F Miller ◽

T E Mandel ◽

...

Keyword(s):

Lymph Nodes ◽

B Lymphocyte ◽

Mononuclear Cells ◽

Plasma Cells ◽

Single Cells ◽

Lymphoid Cells ◽

Membrane Immunoglobulin ◽

Clonal Nature ◽

B Lymphoid

In semisolid agar cultures containing mercaptoethanol, cells from the spleen, lymph nodes, marrow, peritoneal cavity, thoracic duct, and blood of normal mice generated clusters and colonies of up to 3,000 cells. Colony numbers and growth were markedly enhanced by the addition of sheep red cells. The frequency of colony-forming cells in the spleen or lymph nodes was 0.5-2.0%, and cluster forming cells were approximately five times more numerous. The mononuclear cells comprising these colonies had the electronmicroscopic morphology of immature lymphoid and plasma cells. The majority of the cells possessed Fc receptors, 61-69% reacted with anti-mu-serum and 4-11% with anti-gamma2-serum. Analysis of single cells from individual colonies indicated a higher frequency of the cells with membrane immunoglobulin and a clonal pattern of anti-mu or anti-gamma-reactivity. The clonal nature of colonies was supported by an analysis of NIP-binding cells in colonies grown from CBA spleen cells enriched for NIP-binding cells. Mass-harvested colony cells synthesized immunoglobulin in short-term liquid cultures. It is concluded that the colonies are clones of functionally active B-lymphoid cells.

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Ruxolitinib Regulates the Autophagy Machinery in Multiple Myeloma Cells

Anti-Cancer Agents in Medicinal Chemistry ◽

10.2174/1871520620666200218105159 ◽

2020 ◽

Vol 20 (18) ◽

pp. 2316-2323 ◽

Cited By ~ 3

Author(s):

Alican Kusoglu ◽

Bakiye G. Bagca ◽

Neslihan P.O. Ay ◽

Guray Saydam ◽

Cigir B. Avci

Keyword(s):

Multiple Myeloma ◽

Cell Line ◽

B Lymphocyte ◽

Plasma Cells ◽

Annexin V ◽

Myeloma Cell ◽

Control Group ◽

Multiple Myeloma Cell ◽

Ic50 Values ◽

Stat Pathway

Background: Ruxolitinib is a selective JAK1/2 inhibitor approved by the FDA for myelofibrosis in 2014 and nowadays, comprehensive investigations on the potential of the agent as a targeted therapy for haematological malignancies are on the rise. In multiple myeloma which is a cancer of plasma cells, the Interleukin- 6/JAK/STAT pathway is emerging as a therapeutic target since the overactivation of the pathway is associated with poor prognosis. Objective: In this study, our purpose was to discover the potential anticancer effects of ruxolitinib in ARH-77 multiple myeloma cell line compared to NCI-BL 2171 human healthy B lymphocyte cell line. Methods: Cytotoxic effects of ruxolitinib in ARH-77 and NCI-BL 2171 cells were determined via WST-1 assay. The autophagy mechanism induced by ruxolitinib measured by detecting autophagosome formation was investigated. Apoptotic effects of ruxolitinib were analyzed with Annexin V-FITC Detection Kit and flow cytometry. We performed RT-qPCR to demonstrate the expression changes of the genes in the IL-6/JAK/STAT pathway in ARH-77 and NCI-BL 2171 cells treated with ruxolitinib. Results: We identified the IC50 values of ruxolitinib for ARH-77 and NCI-BL 2171 as 20.03 and 33.9μM at the 72nd hour, respectively. We showed that ruxolitinib induced autophagosome accumulation by 3.45 and 1.70 folds in ARH-77 and NCI-BL 2171 cells compared to the control group, respectively. Treatment with ruxolitinib decreased the expressions of IL-6, IL-18, JAK2, TYK2, and AKT genes, which play significant roles in MM pathogenesis. Conclusion: All in all, ruxolitinib is a promising agent for the regulation of the IL-6/JAK/STAT pathway and interferes with the autophagy mechanism in MM.

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Accessory Molecules that Influence Signaling Through B Lymphocyte Antigen Receptors

Advances in Experimental Medicine and Biology - Mechanisms of Lymphocyte Activation and Immune Regulation V ◽

10.1007/978-1-4899-0987-9_4 ◽

1994 ◽

pp. 35-43

Author(s):

Edward A. Clark ◽

Ingolf Berberich ◽

Stephen J. Klaus ◽

Che-Leung Law ◽

Svetlana P. Sidorenko

Keyword(s):

B Lymphocyte ◽

Antigen Receptors ◽

Lymphocyte Antigen ◽

Accessory Molecules

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EVIDENCE FOR IDENTITY OR CLOSE ASSOCIATION OF THE Fc RECEPTOR OF B LYMPHOCYTES AND ALLOANTIGENS DETERMINED BY THE Ir REGION OF THE H-2 COMPLEX

Journal of Experimental Medicine ◽

10.1084/jem.140.3.779 ◽

1974 ◽

Vol 140 (3) ◽

pp. 779-796 ◽

Cited By ~ 125

Author(s):

Howard B. Dickler ◽

David H. Sachs

Keyword(s):

B Lymphocytes ◽

B Lymphocyte ◽

Close Association ◽

Surface Membrane ◽

Fc Receptor ◽

F1 Hybrid ◽

Ia Antigens ◽

Series Of Experiments ◽

Mouse Lymphocytes ◽

Mouse Antibody

Immunoglobulin complexes, composed of heat-aggregated human Ig, were shown to bind to mouse B lymphocytes of a variety of strains, but not to either thymocytes or thymus-derived (T) lymphocytes under a variety of conditions. It was shown that this binding was not due to either natural human antibodies against mouse nor to nonspecific binding of human Ig by mouse lymphocytes. Such complexes were shown to bind to the same sites which bind mouse antibody-antigen complexes. This site is known as the Fc receptor. The binding of Ig complexes to mouse B lymphocytes was markedly inhibited by pretreatment of the lymphocytes with anti-H-2 antisera. A series of experiments indicated the specificity of this result, including the fact that this inhibition was shown not to be due to the artifact of shedding of H-2 antibody-antigen complexes, nor to nonspecific steric inhibition. The antibodies within anti-H-2 antisera which were responsible for this inhibition were specific for alloantigens associated with the Ir region of the H-2 complex (Ia antigens). Antiserum specific for these Ia antigens produced inhibition, whereas antisera specific for antigens determined by the K or D regions of the H-2 complex did not. Evidence was obtained using F1 hybrid cells that at least some Ia antigens of both parental types are expressed on every B lymphocyte (i.e. codominant expression). These data indicate that the Fc receptor and a series of alloantigens controlled by the Ir region of the H-2 complex are identical or closely associated on the B-lymphocyte surface membrane. This observation may have implications for the mechanism of control of the immune response.

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Terapia biológica en enfermedades reumatológicas

Revista Medica Herediana ◽

10.20453/rmh.v24i2.597 ◽

2013 ◽

Vol 24 (2) ◽

pp. 141 ◽

Cited By ~ 1

Author(s):

Manuel F. Ugarte-Gil ◽

Eduardo M. Acevedo-Vásquez ◽

Graciela S. Alarcón

Keyword(s):

T Lymphocyte ◽

B Lymphocyte ◽

Cytotoxic T Lymphocyte ◽

Nuclear Factor Κb ◽

Nuclear Factor ◽

Lymphocyte Antigen ◽

Receptor Activator ◽

B Lymphocyte Stimulator

El advenimiento del uso de terapias biológicas en Reumatología ha modificado significativamente el pronóstico de pacientes portadores de artritis reumatoide (AR), artritis juvenil (AJ), espondilitis anquilosante (EA), entre otras enfermedades. A diferencia de las terapias convencionales estos productos biológicos se dirigen a los llamados blancos terapéuticos ya sea estas una línea celular, un mediador inflamatorio o un receptor de superficie. Estos compuestos son producidos por células vivas mediante la tecnología del ADN recombinante. Estos compuestos pueden tener componentes humano y animal [quiméricos (Xi), humanizados (Zu)], o completamente humanos (H) lo cual se reconoce por las letras que se incluyen en el nombre de cada uno. En el campo de la Reumatología, el primer compuesto utilizado fue el etanercept (anti-factor de necrosis tumoral o anti-TNF) aprobado en 1998, pero otros anti-TNF han demostrado su beneficio en AR, como en EA y AJ. Los inhibidores de Interleucina (IL-1) casi no se usan en AR actualmente, pero si los inhibidores de IL-6, así como los agentes contra las células B y los agonistas de CTLA-4 (Cytotoxic T lymphocyte antigen). Existe asimismo un compuesto dirigido al BLyS (B-lymphocyte stimulator) el cual se usa en lupus eritematoso sistémico y otro dirigido al receptor activador del factor nuclear κB (RANKL, receptor activator of nuclear factor-κB ligand) que se usa en osteoporosis. Con el avance en el conocimiento de la patogenia de las enfermedades reumáticas, se vienen reconociendo otra blancos terapéuticas. En los años venideros, este campo ha de expandirse en proporciones geométricas.

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