Construction of an antigenic map for human B-cell precursors

Melink, Georgiann B.; LeBien, Tucker W.

doi:10.1007/bf00915350

Cited by 20 publications

(6 citation statements)

References 28 publications

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“…The human CD24 antigen is expressed on the surface of B-cell precursors but is lost with the onset of plasma cell differentiation (Melink and Lebien, 1983). It was originally described on mature granulocytes (Knapp et al.…”

mentioning

confidence: 99%

Expression of a B‐cell marker, CD24, on nasopharyngeal carcinoma cells

Karran¹,

Jones²,

Morley³

et al. 1995

Intl Journal of Cancer

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Random sequencing of clones from a lambda gt10 cDNA library, made from mRNA expressed in an Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma (NPC) has revealed the gene transcript of human CD24. The CD24 antigen, a glycosylphosphatidylinositol-anchored cell surface molecule, has been identified as a B-cell marker that is lost during cell maturation. We show here that it is expressed on 3 NPC xenografts, previously defined as consisting of poorly differentiated epithelial cells, and on an NPC biopsy. In the case of the former, the level of expression of CD24 corresponds to the EBV load. A B-lymphoblastoid cell line carrying the same EBV genome as one of the tumours, C15, and an EBV-negative Burkitt's lymphoma cell line do not display the antigen, but epithelial-like cells of a laryngeal tumour cell line (Hep2) do express it. Our data suggest that CD24 may be a marker of cell differentiation not only for B cells but also for epithelial cells and may have an indirect association with EBV gene expression.

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mentioning

confidence: 99%

Expression of a B‐cell marker, CD24, on nasopharyngeal carcinoma cells

Karran¹,

Jones²,

Morley³

et al. 1995

Intl Journal of Cancer

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“…Although we observed a deficiency of sIg B cells in PBL of myeloma patients, we were surprised to find that the number of BA-1+ cells was normal or supranormal in most patients (66). BA-1 is a marker for B and pre-B cells defined by a monoclonal antibody raised against a pre-B leukemia cell line (67)(68)(69). In normal PBL, essentially all BA-1+ cells are also sIg+ (68); this was confirmed by our own analysis Using double IF, these BA-1 + cells in patient PBL were shown to be sIg-, cytoplasmic IgM+ (cIgM+) cells that were not monocytes or granulocytes.…”

Section: Pre-b Cells In the Blood Of Multiple Myeloma Patientsmentioning

confidence: 79%

“…BA-1 is a marker for B and pre-B cells defined by a monoclonal antibody raised against a pre-B leukemia cell line (67)(68)(69). In normal PBL, essentially all BA-1+ cells are also sIg+ (68); this was confirmed by our own analysis Using double IF, these BA-1 + cells in patient PBL were shown to be sIg-, cytoplasmic IgM+ (cIgM+) cells that were not monocytes or granulocytes.…”

Section: Pre-b Cells In the Blood Of Multiple Myeloma Patientsmentioning

confidence: 99%

Analysis of immunodeficiency in multiple myeloma: Observations and hypothesis

Pilarski

Mant

Ruether

1987

Clinical Laboratory Analysis

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Patients with multiple myeloma suffer from often profound immunodeficiency that seriously compromises both longevity and quality of life. The cellular basis for the immunodeficiency is unknown and the mechanism(s) giving rise to and possibly maintaining it is also unknown. In this review, evidence defining cellular defects in the nonmalignant B and T peripheral blood lymphocyte pool is summarized and discussed in terms of possible mechanisms that could give rise to the abberrant immune phenotype characteristic of many patients. The abnormalities we have defined include a deficiency of mature B lymphocytes, presence of often large numbers of pre-B cells in the blood, arrested differentiation of B cells into immunoglobulin (Ig)-secreting cells, and abnormal progenitorlike T cells in blood. The specificity repertoire of the remaining B lymphocyte population is heavily skewed toward recognition of idiotypic and shared epitopes on the variable region of Ig, perhaps reflecting immune reaction with the monoclonal myeloma lg. This may begin as a response to tumor antigen that gradually progresses to autoimmunity. A second subset of B cells present at abnormally high frequency in myeloma patients is that of antigen-experienced memory B cells, which probably encountered antigen prior to the events leading to frank myeloma. In this instance, the high frequency reflects a decrease in aggregate numbers of B cells, although it seems likely that expansion of memory clones also occurs. This is exemplified by the set of memory B cells specific for tetanus toxoid, which are present at normal number but highly enriched frequency in myeloma PBL. Both the antitumor B cells (anti-idiotype, and anti-lg) and the memory cells specific for environmental pathogens appear to be arrested in their differentiation to 19-secretors as evidenced by the lack of serum antibody in patients. The above observations are interpreted in terms of the hypothesis that immunoregulatory events triggered by the monoclonal myeloma lg establish and maintain the immunodeficiency. We speculate that autoimmune suppressor T cells specific for conserved determinants of Ig prevent pre-B cell differentiation to slg+ B cells, and B cell terminal differentiation to Ig-secretors. If correct, this analysis could lead to therapeutic approaches for the reversal of the immunodeficiency and perhaps some degree of control over the malignant growth.

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“…The molecule was assigned its CD designation al Ihe Second I.eukoeyte Workshop [5]. It has been demonstrated to be expressed on human B lymphocytes from precursors up lo before the onset of plasma cell differentiation [6]. on mature granulocytes [7], on epithelial cells ofthe renal giomerulus and tubulus [8] and on lumour cell lines, including leukaemia, lymphoma, astrocytoma, neurobiastoma and melanoma [9].…”

Section: Introductionmentioning

confidence: 99%

Antibodies to the protein core of the small cell lung cancer workshop antigen cluster-w4 and to the leucocyte workshop antigen CD24 recognize the same short protein sequence leucine-alanine-proline

Weber

Lehmann

Beck‐Sickinger

et al. 1993

Clinical and Experimental Immunology

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SUMMARYWe recently described the identity of Ihe small cell lung cancer (SCI.C) cluster-w4 antigen and the human B cell ditlcrentiation marker CD24, a glycosylphosphatidylinosilol (GPI)-anchored, highly glycosylalcd surface molecule ofonly 31 -35 amino acids [15]. The specificities of three anti-cluster-w4 and of eleven anti-CD24 MoAbs have been investigated with respect to their binding capacity lo the protein core of cluster-w4/CD24 antigen. Four overlapping peptides spanning ihis protein core were synthesized. MoAbs shown to bind to two overlapping peptides by antibody binding inhibition using the cluster-w4/CD24-positive SCLC cell line SW2 and by direct peptide binding detecied in an ELISA were investigated in more detail. To determine the exact epitopes recognized by these MoAbs. an epitope mapping assay using peptides synthesized onto polyethylene pins was established. The three anti-cluster-w4 MoAbs SWA 11, SWA2I and SWA22 and the anti-CD24 MoAbs OKB2 and ALB9 recognized the same short leucine-alanine-proline (LAP) sequence in an area without potential glycosytation sites close lo the GPI anchor oi the protein core of the cluster-w4/CD24 antigen.Keywords epitope mapping monoclonal aniibody SWA 11 clusler-w4 antigen CD24 antigen small cell lung cancer

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Construction of an antigenic map for human B-cell precursors

Cited by 20 publications

References 28 publications

Expression of a B‐cell marker, CD24, on nasopharyngeal carcinoma cells

Expression of a B‐cell marker, CD24, on nasopharyngeal carcinoma cells

Analysis of immunodeficiency in multiple myeloma: Observations and hypothesis

Antibodies to the protein core of the small cell lung cancer workshop antigen cluster-w4 and to the leucocyte workshop antigen CD24 recognize the same short protein sequence leucine-alanine-proline

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