Human B cell variants immunoselected against a single Ia antigen subset have lost expression of several Ia antigen subsets.

Two monoclonal antibodies, D1-12 and BT 2.2, recognizing two distinct subsets of human Ia molecules, NG1 and NG2, respectively, present in all individuals irrespective of their HLA-DR phenotype, have been used to immunoselect cell variants from the lymphoblastoid cell line Raji. Results showed that, irrespective of the monoclonal antibody used for immunoselection, the cell variants analyzed in this study had lost the expression of both D1-12-and BT 2.2-specific antigenic determinants. Moreover, the expression of antigenic determinants specific for a third family of Ia molecules, the DC-1 subset, were also lost in the cell variants. In contrast, expression of HLA A, B, and C common structures, as recognized by the W6.32 monoclonal antibody, as well as expression of surface immunoglobulins, were not affected. Possible mechanisms inducing such a coordinate loss of expression of several families of human Ia molecules are discussed.

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Direct demonstration of an HLA-DR allotypic determinant on the low molecular weight (beta) subunit using a mouse monoclonal antibody specific for DR3

Journal of Experimental Medicine ◽

10.1084/jem.156.1.104 ◽

1982 ◽

Vol 156 (1) ◽

pp. 104-111 ◽

Cited By ~ 55

Author(s):

JP Johnson ◽

T Meo ◽

G Reithmuller ◽

DJ Schendel ◽

R Wank

Keyword(s):

Molecular Weight ◽

Monoclonal Antibody ◽

Cell Surface ◽

B Cell ◽

Beta Subunit ◽

Low Molecular Weight ◽

Β Subunit ◽

Direct Demonstration ◽

Hla Dr ◽

Human B Cell

A murine monoclonal antibody directed against a human B cell surface antigen with the characteristics of HLA-DR is described. The antigen detected is tightly linked to HLA and is correlated with the alloantigen HLA-Dw/DR3. Reactivity with a fraction of Dw/DRw6 cells is also observed. The determinant recognized by this antibody has been shown to be present on the smaller molecular weight β subunit of the HLA-DR antigen.

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The Protein Kinase C-Independent Human B Cell Proliferation Induced via Surface Immunoglobulins is Unaffected by CD45 Monoclonal Antibodies

Immunobiology ◽

10.1016/s0171-2985(11)80199-3 ◽

1991 ◽

Vol 182 (2) ◽

pp. 152-160

Author(s):

Jûlia Ingles-Esteve ◽

Francisco Lozano ◽

Montserrat Plana ◽

Jose Alberola-Ila ◽

Lourdes Places ◽

...

Keyword(s):

Cell Proliferation ◽

Monoclonal Antibodies ◽

Protein Kinase C ◽

Protein Kinase ◽

B Cell ◽

Kinase C ◽

Surface Immunoglobulins ◽

Human B Cell

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Comparison between two kinds of cigarette smoke condensates (CSCs) of the cytogenotoxicity and protein expression in a human B-cell lymphoblastoid cell line using CCK-8 assay, comet assay and protein microarray

Mutation Research/Genetic Toxicology and Environmental Mutagenesis ◽

10.1016/j.mrgentox.2010.01.014 ◽

2010 ◽

Vol 697 (1-2) ◽

pp. 55-59 ◽

Cited By ~ 26

Author(s):

Jianlin Lou ◽

Guohai Chu ◽

Guojun Zhou ◽

Jian Jiang ◽

Fangfang Huang ◽

...

Keyword(s):

Comet Assay ◽

Protein Expression ◽

B Cell ◽

Cell Line ◽

Cigarette Smoke ◽

Lymphoblastoid Cell Line ◽

Protein Microarray ◽

Human B Cell

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Acute lymphoblastic leukemia in infants: evidence for B cell origin of disease by use of monoclonal antibody phenotyping

Blood ◽

10.1182/blood.v68.4.975.975 ◽

1986 ◽

Vol 68 (4) ◽

pp. 975-978 ◽

Cited By ~ 20

Author(s):

PA Dinndorf ◽

GH Reaman

Keyword(s):

Monoclonal Antibody ◽

Monoclonal Antibodies ◽

Stem Cell ◽

Acute Lymphoblastic Leukemia ◽

B Cell ◽

Lymphoblastic Leukemia ◽

B Cell Development ◽

Lymphoid Cells ◽

Hla Dr ◽

Cell Commitment

Abstract Since the prognosis of infants with acute lymphoblastic leukemia (ALL) is so poor, it has been suggested that these leukemias may not be lymphoid in origin, but may originate from stem cell, myeloid, or megakaryocytic progenitors. Alternately it has been hypothesized that these leukemias originate in lymphoid cells at the earliest stages of B cell development. Another possibility is that these leukemias may be of more than one lineage. Therefore we examined leukemic blasts from 12 infants with ALL using monoclonal antibodies to myeloid and lymphoid differentiation antigens. The majority of specimens expressed HLA/DR and reacted with B4 (CD19) but failed to react with stem cell, myeloid, megakaryocytic, or T cell associated antibodies. These results support the speculation that the majority of these leukemias arise in cells at the earliest stages of B cell commitment, and are not of a myeloid or biphenotypic nature.

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Translation and assembly of HLA-DR antigens in Xenopus oocytes injected with mRNA from a human B-cell line.

The EMBO Journal ◽

10.1002/j.1460-2075.1982.tb01222.x ◽

1982 ◽

Vol 1 (5) ◽

pp. 649-654 ◽

Cited By ~ 17

Author(s):

E.O. Long ◽

N. Gross ◽

C.T. Wake ◽

J.P. Mach ◽

S. Carrel ◽

...

Keyword(s):

B Cell ◽

Cell Line ◽

Xenopus Oocytes ◽

Hla Dr ◽

Human B Cell

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CHIR-12.12, an Antagonist Anti-CD40 Antibody, Exhibits Greater ADCC Than Rituximab Against a Variety of Malignant B Cells: Evaluation of FcγRIIIa Polymorphism and ADCC Response.

Blood ◽

10.1182/blood.v106.11.1472.1472 ◽

2005 ◽

Vol 106 (11) ◽

pp. 1472-1472

Author(s):

Mohammad Luqman ◽

Xia Tong ◽

Xiaohong Niu ◽

Pablo Garcia ◽

Michel Faure ◽

...

Keyword(s):

Monoclonal Antibody ◽

B Cell ◽

Nk Cells ◽

Cell Line ◽

Cell Lines ◽

Cell Lysis ◽

Target Cells ◽

Adcc Activity ◽

Phase I Clinical Trials ◽

Human B Cell

Abstract We have generated a novel, fully human IgG1 anti-CD40 antagonistic monoclonal antibody, CHIR-12.12, using XenoMouse® mice (Abgenix, Inc.) and have previously demonstrated that it inhibits normal human B cell proliferation and survival and has potent ADCC against primary CLL and NHL cells. CHIR-12.12 and the anti-CD20 monoclonal antibody rituximab were compared for their relative ADCC activity against a variety of malignant human B-cell lines expressing both CD40 and CD20 antigens, including two lymphoma cell lines (Daudi, Namalwa), two multiple myeloma cell lines (ARH77, IM-9), a B-ALL cell line (CCRF-SB), and a B-CLL cell line (EHEB). All cell lines expressed both CD20 and CD40 antigens, and the number of cell surface CD20 molecules per cell were 2.6- to 30.8-fold higher than CD40. For all target cell lines, despite the greater number of CD20 receptors, CHIR-12.12 showed greater maximum cell lysis and a lower ED50 than rituximab. ADCC activity of rituximab is known to correlate with the FcγRIIIa genotype of the effector cells. The homozygous valine (V/V) or heterozygous valine/phenylalanine (V/F) polymorphisms at aa158 are associated with greater cell lysis than is the homozygous F/F polymorphism. The role of the FcγRIIIa aa158 genotype as it relates to CHIR-12.12 activity was explored using Daudi lymphoma target cells and effector NK cells purified from human donors expressing the three polymorphisms. CHIR-12.12 induced potent ADCC with NK cells of all three genotypes (ED50s of 4, 2, and 0.4 pM for F/F, V/F, and V/V, respectively). The rituximab ED50s were 53, 21, and 9 pM for F/F, V/F, and V/V, respectively. Comparison of affinity of the FcγRIIIa F and V alleles for CHIR-12.12 and rituximab using Biacore® analysis showed that CHIR-12.12 bound the F allele with a 4.6-fold higher affinity than rituximab (2.8 μM versus 13 μM, respectively). These data demonstrate that CHIR-12.12 is a more potent ADCC mediator than rituximab, even with human NK cells of the aa158 F/F genotype. CHIR-12.12 is currently in Phase I clinical trials for B-cell malignancies.

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Acute lymphoblastic leukemia in infants: evidence for B cell origin of disease by use of monoclonal antibody phenotyping

Blood ◽

10.1182/blood.v68.4.975.bloodjournal684975 ◽

1986 ◽

Vol 68 (4) ◽

pp. 975-978

Author(s):

PA Dinndorf ◽

GH Reaman

Keyword(s):

Monoclonal Antibody ◽

Monoclonal Antibodies ◽

Stem Cell ◽

Acute Lymphoblastic Leukemia ◽

B Cell ◽

Lymphoblastic Leukemia ◽

B Cell Development ◽

Lymphoid Cells ◽

Hla Dr ◽

Cell Commitment

Since the prognosis of infants with acute lymphoblastic leukemia (ALL) is so poor, it has been suggested that these leukemias may not be lymphoid in origin, but may originate from stem cell, myeloid, or megakaryocytic progenitors. Alternately it has been hypothesized that these leukemias originate in lymphoid cells at the earliest stages of B cell development. Another possibility is that these leukemias may be of more than one lineage. Therefore we examined leukemic blasts from 12 infants with ALL using monoclonal antibodies to myeloid and lymphoid differentiation antigens. The majority of specimens expressed HLA/DR and reacted with B4 (CD19) but failed to react with stem cell, myeloid, megakaryocytic, or T cell associated antibodies. These results support the speculation that the majority of these leukemias arise in cells at the earliest stages of B cell commitment, and are not of a myeloid or biphenotypic nature.

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