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PubMed1983

Studies on the B lymphoblast antigen No. 1 (BB-1) on a series of Burkitt lymphoma lines differing in the expression of the EBV/C3 receptor complex.

In the Jijoye-P3HR-1 family of Burkitt lymphoma sublines, the expression of the B lymphoblast-1 antigen, BB-1, identified by the monoclonal antibody described by Yokochi and colleagues, was found to be strictly related to the expression of the EBV receptor/C3 receptor (EBVR/C3R) complex. It was absent on the receptor-negative P3HR-1 line, present in the original receptor-positive Jijoye line, and reappeared in nonvirus producer sublines derived from P3HR-1 itself. We suggest the BB-1 antigen is related to the EBVR/C3R complex in the Jijoye family, either at the level of genetic or epigenetic determination or at the level of steric interaction on the cell membrane. In all probability, however, the BB-1 antigen is not identical to the receptor itself. It is also clear that a similar relationship does not necessarily apply to other cell lines. In the course of the studies, it was accidentally discovered that propagation of the P3HR-1 cells on newborn instead of fetal calf serum induces the concomitant expression of EBV receptors, C3 receptors, and the BB-1 antigen. The mechanism of this induction is obscure; it does not appear to be related to any significant change in the frequency of virus-producing cells.

Animals↗

PubMed1983

Studies of the Epstein Barr virus receptor found on Raji cells. II. A comparison of lymphocyte binding sites for Epstein Barr virus and C3d.

A comparison was made between the binding sites of two receptors that are believed to be closely associated on human B lymphocytes: complement receptor type two (CR2) that is specific for C3d fragments, and the receptor (EBVR) for Epstein Barr virus (EBV). Isolated fluid-phase CR2 bound to C3d on erythrocytes (EC3d) and inhibited both B cell-EC3d rosettes and the agglutination of EC3d by anti-C3d, it failed to inhibit either the binding or superinfection of B cells by EBV. By contrast, isolated fluid-phase EBVR inhibited EBV B cell binding activity and superinfection but had no CR2 activity. In addition, radiolabeled CR2 bound to EC3d and anti-CR2-Sepharose, whereas radiolabeled EBVR did not. Purified fluid-phase C3d fragments inhibited EC3d rosette formation with CR2+/EBVR+ cells but did not inhibit EBV binding. However, EBV binding to B cells did inhibit EC3d rosette formation. Clones of human/mouse somatic cell hybrids made from CR2+/EBVR+ human B lymphoblastoid cell and CR2-/EBVR- mouse myeloma cell parents expressed either EBVR or CR2 but only rarely expressed both EBVR and CR2. This suggested that the genes for EBVR and CR2 were located on two different human chromosomes. Thus it was concluded that CR2 is probably not the binding site for EBV.

Animals↗

PubMed1983

Studies of the Epstein-Barr virus receptor found on Raji cells. I. Extraction of receptor and preparation of anti-receptor antibody.

Raji, a human lymphoblastoid cell line, expresses a membrane receptor (EBVR) specific for Epstein Barr virus (EBV). A component that binds EBV was extracted from this cell line by treatment of the cells for 3 hr on ice with Tris buffer containing 10% glycerol. The treatment reduced the capacity of the cells to bind virus, and after concentration the receptor extract (RE) inhibited both EBV binding and superinfection of fresh Raji cells. Similarly prepared extracts of EBVR- cells lacked such activity. An antibody was made to the extract (anti-RE), which after absorption with EBVR- cells, bound to the same percentages of EBVR+ lymphoblastoid cell lines, EBVR+ human/mouse somatic cell hybrids, and fresh peripheral B cells as the virus did. In reciprocal assays, preincubation of EBVR+ cells with anti-RE inhibited virus binding. Doubly stained patches were observed on membranes of EBVR+ cells that had been incubated simultaneously with virus and anti-RE and stained respectively with rhodaminated and fluoresceinated reagents. The major polypeptide immunoprecipitated by anti-RE from radiolabeled Raji cells had an approximate calculated m.w. of 150,000.

Animals↗

PubMed1983

Deficiency in Epstein-Barr virus receptors on B-lymphocytes of preleukemia patients.

Lymphocytes from eight preleukemia patients were exposed to Epstein-Barr virus (EBV) in vitro in an attempt to establish lymphoblastoid cell lines. No signs of viral infection were detected, and no cell lines were obtained. Studies using fluorescein-labeled EBV and flow cytometry revealed an unusual and consistent deficiency in EBV receptors in all patients examined. In control studies, about 15% of the unseparated lymphocytes from healthy donors bound fluorescein-labeled EBV. In spite of the lack of EBV receptors, B-lymphocytes amounted to 10 to 20% of the preleukemia lymphocyte populations, a proportion similar to that in healthy donors. When lymphocytes from preleukemic patients were first implanted with functional EBV receptors and then exposed to EBV, synthesis of EBV-determined nuclear, early, and viral capsid antigens was induced. Subsequently, several cell lines originating from preleukemic patients' lymphocytes were established. These lines are of a B-lymphocyte origin and carry EBV genome. They will provide experimental material for the molecular analysis of lymphocytic defects in preleukemia and their possible role in the transition to acute leukemia.

B-Lymphocytes↗

PubMed1994

Stimulation of human IgE production by a subset of anti-CD21 monoclonal antibodies: requirement of a co-signal to modulate epsilon transcripts.

CD21, the receptor for Epstein-Barr virus (EBV) and the complement receptor-2 (CR2), was recently found to interact specifically with CD23, a low-affinity receptor for IgE, and to regulate IgE production. Therefore, the effect of different anti-CD21 monoclonal antibodies (mAb) on IgE synthesis by blood mononuclear cells was investigated. One anti-CD21 mAb, BU-33, was able to increase significantly (more than threefold) interleukin-4 (IL-4)-induced IgE synthesis, whereas HB-5, OKB-7 and B2 anti-CD21 mAb had no effect. BU-33 had no effect on IgG and IgA production and produced only a moderate increase in IgM production. Recombinant, 29,000 MW, soluble CD23 (sCD23) expressed in COS cells exhibited the same IgE-enhancing activity. BU-33 was the best inhibitor of CD23-liposome binding to the CD21-positive cell line RPMI-8226 when compared to the other anti-CD21 mAb tested. BU-33 identified a different epitope on CD21. The effect of BU-33 on IgE production by purified tonsillar B cells and highly purified germinal centre B cells, was dependent on the presence of T cells or anti-CD40 mAb stimulation. Molecular analysis revealed that BU-33 alone failed to induce germline epsilon mRNA but increased the IL-4-induced germline epsilon transcription levels. Moreover, BU-33 had a synergistic effect on anti-CD40 mAb or T-cell-induced productive epsilon transcript expression. These results therefore indicate that the CD23-CD21 interaction needs a co-signal for B-cell differentiation towards IgE production.

Antibodies, Monoclonal↗

PubMed1994

CD23 interacts with a new functional extracytoplasmic domain involving N-linked oligosaccharides on CD21.

Human CD21 has been described as a receptor for the C3d,g and iC3b proteins of complement, for the Epstein-Barr virus, and also for IFN-alpha. We reported recently that CD23, a low affinity receptor for IgE (Fc epsilon R2), is a new functional ligand for CD21. To determine the site of interaction of CD23 on CD21, we analyzed the ability of purified recombinant CD23 incorporated into fluorescent liposomes to bind CD21 mutants bearing various deletions of extracytoplasmic short consensus repeats (SCRs). We found that the site of interaction of CD23 on CD21 is on SCRs 5 to 8, with contribution of SCRs 1 and 2. Tunicamycin treatment of CD21-transfected K562 cells strongly inhibited the binding of CD23-liposomes, suggesting that an N-linked sugar, present on SCRs 5 to 8, is involved in the CD23/CD21 interaction. By mutating together or individually, the three asparagines present on SCRs 5 to 8, asparagines (Asn) 370 and 295, but not Asn 492, were shown to be involved critically in the binding of CD23. Furthermore, we mapped the binding sites of a panel of anti-CD21 mAbs and found that at least six epitopes can be detected on CD21. The mAbs that inhibit the most CD23 binding to CD21 map in SCRs 5 to 8. This study indicates that SCRs 5 to 8 represent a novel functional domain on the CD21 molecule, and is the first demonstration of an activity of an extracytoplasmic region of the CD21 outside of SCRs 1 to 4.

Antibodies, Monoclonal↗

PubMed1994

[Regulation of the production of IgE in man].

Allergy is associated with elevated production of allergen-specific IgE antibody. Naive allergen-specific B cells undergo a series of molecular interactions before they would produce allergen-specific IgE antibody. Besides allergen recognition, specific B cells have to receive signals from cell-surface proteins and cytokines from their various cellular partners. Activated T cells express a ligand for CD40 that rescues germinal centre B cells from programmed cell death. Contact with follicular dendritic cells or other T and B cells promotes differentiation into plasma through engagement of two pairs of complementary cell-surface proteins, CD21/CD23. Among the many cytokines secreted by helper T cells, interleukin-4 is necessary for the class switch to IgE, and IL-13 also triggers switching to IgE. Then, IgE would participate to feed-back regulation of its production by acting at different levels. When bound to CD23, also known as Fc epsilon receptor type II, IgE immune complexes inhibit CD21/CD23 cell-cell interactions. When bound to Fc epsilon receptor type I on Langerhans' cells in the skin or mucosa, IgE antibody enhances allergen presentation to T cells and promotes their differentiation into type 2 helper T cells that secrete IL-4 but no interferon-gamma. Local activation of mast cells or basophils, via their Fc epsilon Receptor type I-bound IgE, would trigger secretion of various cytokines, IL-4 in particular, and expression of CD21 and CD40 ligand, which altogether could replace contact with T cells to deliver the co-stimulatory signals for localised IgE production.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigens, CD↗

PubMed1995

The B lymphocyte as an immunotherapeutic target.

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Antigens, CD↗

PubMed1993

Relation of follicular dendritic reticulum cells to Reed-Sternberg cells of Hodgkin's disease with emphasis on the expression of CD21 antigen.

Based on observations of 66 cases, in which tissues were specially processed to optimize the simultaneous preservation of cell membrane antigens and morphology, we provide evidence in favor of a relationship between follicular dendritic reticulum cells (FDRC) and Reed-Sternberg (RS) cells of Hodgkin's disease (HD) other than the lymphocyte predominance subtype. RS cells were intimately related to the FDRC network (75% of cases), and the expression of CD21 antigen was frequent (41% of cases). Exclusive expression of CD21 antigen was found in 11 cases of HD, while the expression of other B-cell-associated markers (CD19, CD20, CD22) was both variable and inconsistent. The expression of T-cell antigens (CD3, CD4, CD8) was rare. Null phenotype of RS cells was observed in 27 of 66 cases (41%). Epstein-Barr virus (EBV) nucleic acids were found in 34 of 66 (51.5%) cases. Double labeling techniques showed the presence of EBV-positive RS cells within the FDRC network. A non-B-cell origin of RS cells was supported by the differential expression of EBV latent antigens in HD (latent membrane protein+, EB nuclear antigen 2-), which is unusual in EBV-driven lymphoblastoid cell lines and EBV-positive B-cell lymphomas. FDRC and RS cells are known to share morphological traits (binucleated cells), and both cell types possess Fc receptor for IgG. The hypothesis is further backed by the findings of CD15 antigen expression by occasional RS-like dysplastic FDRC in Castleman's disease (five cases), which is characterized by hyperplasia of FDRC. Whether FDRC might be the only cells involved in the conversion to RS cells by the loss or gain of antigens remains to be determined.

Antibodies↗

PubMed1995

Model of Epstein-Barr virus infection of human thymocytes: expression of viral genome and impact on cellular receptor expression in the T-lymphoblastic cell line, HPB-ALL.

Infection of B lymphocytes and epithelial tissue by Epstein-Barr virus (EBV) is associated with malignancy and autoimmunity. The cellular receptor for EBV has been identified as CD21 (CR2). A molecule, which is biochemically and immunologically similar to B-cell CD21, has been identified on a subpopulation of immature thymocytes, suggesting a role for this molecule in the regulation of T-cell development and further suggesting that immature T cells might be susceptible to EBV infection. A growing body of literature now documents the presence of EBV in tumors of T-cell origin. We have evaluated the susceptibility of the human immature T cell line, HPB-ALL, to infection by EBV. Electron microscopy studies showed a rapid internalization of virus by HPB cells. Southern blotting showed the intracellular presence of linear EBV genomes, and components of the virus replicative cycle were identified. Expression of the BamHI Z region of the genome, encoding the nuclear protein, ZEBRA, which is strictly associated with productive infection in B cells, was detected in HPB-ALL cells. A spliced variant of Z, RAZ, was also identified. Cell surface expression of EBV late antigens was observed to occur transiently. Infection of HPB cells was also accompanied by altered expression of T-cell surface molecules involved in antigen recognition, a process critical to normal development of the T-cell repertoire. Delineation of the outcome of T-cell infection by EBV may lead to a better understanding of the role of this virus in autoimmune processes and malignancy.

Autoimmune Diseases↗

PubMed1994

Characterization of a 70-kDa, EBV gp350/220-binding protein on HSB-2 T cells.

EBV binds and infects HSB-2 T cells via a receptor distinct from CD21. To further study this novel EBV receptor, we expressed the first 470 amino acids of the EBV-gp350/220 using the baculovirus expression system. The recombinant gp350/220(1-470) has a m.w. of 95 kDa, reacts with anti-gp350/220 Abs, and binds CD21 in ELISA. Radiolabeled gp350/220(1-470) binds both HSB-2 and Raji cells. The gp350/220(1-470) protein also inhibits EBV binding to both HSB-2 and Raji, detected by flow cytometry. Lysates of HSB-2 cells compete with CD21 for binding to gp350/220(1-470), suggesting that the two receptors bind related epitopes on the recombinant protein. Scatchard analysis reveals that gp350/220(1-470) binds to 34,000 high affinity sites/HSB-2 cell (Kd = 0.92 x 10(-8) M) compared with the 97,000 high affinity sites bound/Raji cell (Kd = 1.78 x 10(-8) M). Utilizing a gp350/220(1-470)-affinity matrix, we identify a 70-kDa (55-kDa nonreduced) protein on the surfaces of 125I-labeled HSB-2 cells. Binding of this protein to the matrix is inhibited by anti-gp350/220 Ab 72A1. In summary, we characterize a novel EBV-binding molecule on HSB-2 cells, compare its reactivity with gp350/220 to that of CD21, and provide evidence of a gp350/220-reactive, 70-kDa protein on the surfaces of HSB-2 cells. In view of previous evidence of HSB-2 infectivity by EBV, we propose that the 70 kDa protein represents the novel EBV receptor.

Animals↗

PubMed1993

Transient expression of the Epstein-Barr virus LMP1 gene in B-cell chronic lymphocytic leukemia cells, T cells, and hematopoietic cell lines: cell-type-independent-induction of CD23, CD21, and ICAM-1.

The Epstein-Barr virus (EBV) genome has recently been detected in various non-B cell neoplasms, including various T-cell leukemias and in Reed-Sternberg cells of Hodgkin's disease, but the contribution of EBV genes to the transformed phenotype remains unclear. We have investigated the possible effect which the EBV genes LMP1 and EBNA2, of which the expression has been reported in non-B cell neoplasms, may have on a variety of cell types. The LMP1 and EBNA2 genes were transiently expressed from heterologous promoters in two human T-cell lines (HPB-ALL and Jurkat), two human cell lines of the myeloid lineage (K562 and U937), one type I Burkitt's lymphoma cell line (Rael) and in human primary T cells and B-cell chronic lymphocytic leukemia cells. The cell surface expression of CD23, CD21, ICAM-1 and LFA-1 was monitored on transfected cells. In the cell lines, except U937, the surface antigens CD21 and ICAM-1 were upregulated in a dose-dependent and transient manner by the transient expression of LMP1, and EBNA2 slightly enhanced the effects of LMP1 on CD23 and CD21 upregulation. LMP1 also induced increased CD21, ICAM-1 and LFA-1 surface expression on transfected primary T-cells, and CD21 and ICAM-1 in four of five B-cell chronic lymphocytic leukemias tested. Finally, LMP1 transient expression caused increased cell size of the primary T cells and responding B-cell chronic lymphocytic leukemia cells. Our results strongly suggest that LMP1 can trigger specific responses in a variety of white cell types and thus is probably contributing to the phenotype of EBV-positive tumor cells not only in the B-cell lineage.

Antigens, Viral↗

PubMed1994

Expression and tumorigenicity of the Epstein-Barr virus BARF1 gene in human Louckes B-lymphocyte cell line.

We previously showed that the Epstein-Barr virus, which encodes the BARF1 gene, could transform rodent fibroblasts. In this work, the expression of the BARF1 gene was studied in the human Louckes B-lymphocyte cell line. Introduction of the BARF1 open reading frame under the control of the Mo-MuLV LTR promotor into nontumorigenic Louckes lymphoid cells led to the activation of the c-myc protooncogene and increased expression of the B-cell surface proteins, the transferrin receptor, CD21, and CD23. BARF1-expressing cells induced a diffuse lymphoma-like tumor in newborn rats treated with anti-thymocyte serum that was, however, transient and regressed after 3-4 weeks as the immune system recovered. The tumor induction was similar to that observed with lymphoid cell lines in vitro generated by infection with the B95-8 virus strain, in which lytic antigens are expressed at low levels. After long-term culture, Louckes cell clones lost expression of the BARF1 gene and were unable to induce tumors.

Antigens, CD↗

PubMed1994

CD23/IgE-mediated regulation of the specific antibody response in vivo.

We have recently reported that IgE Abs specific for TNP are able to enhance the specific IgG response in mice via the low affinity receptor for IgE, Fc epsilon RII, or CD23. In this study we show that IgE can up-regulate IgM, IgG1, IgG2a, and the IgE response, thereby indicating the possibility of a viscious circle in the maintenance of an allergic response. One of the suggested modes of action of IgE/CD23 is to increase the ability of B cells to present Ag to T cells. The involvement of T cells in IgE-mediated enhancement of the Ab response was studied in several ways: nude mice were resistant to the effect of IgE and a dramatic effect on the induction of immunologic memory was seen, both by in situ secondary immunizations and in adoptive transfer systems. Basic conditions for the ability of IgE to induce enhancement were established, demonstrating critical importance of factors such as type of Ag and temporal relationship between administration of IgE and Ag. Finally, no evidence for the requirement for CD23 for a normal (non-IgE induced) Ab response was found, although modulation of the receptor completely abrogated the IgE-induced Ab response.

Animals↗

PubMed1994

Role of IL-6 in promoting growth of human EBV-induced B-cell tumors in severe combined immunodeficient mice.

To investigate the role of IL-6 as a growth factor in EBV-induced B lymphoproliferative disorders in immune-suppressed patients, we analyzed two B cell lines derived from two different patients for IL-6 production, expression of the p80 chain of the IL-6 receptor, and the effects on cell growth in vitro and in vivo of neutralizing mAbs specific for IL-6. One of the cell lines (LCL41) was shown to produce large amounts of IL-6 and to express IL-6 receptors. Its in vitro growth was weakly inhibited by the anti-IL-6 MAb. After inoculation into SCID mice, this cell line provoked human B cell tumors, the growth of which was controlled by the anti-IL-6 mAb. Indeed, four i.v. infusions of 0.1 mg at days 30 to 42 after i.p. inoculation of cells led to complete remission in most mice and long term survival in 40% of cases. In contrast, the other B cell line (LCL48) produced smaller amounts of IL-6; its growth was not inhibited in vitro by the anti-IL-6 Ab and was poorly blocked in vivo in SCID mice (40% of remissions and 20% of long-term survival). In addition, a clone derived in vivo in SCID mice from LCL48 was completely IL-6-independent. These results demonstrate that B cell tumors transformed in vivo by EBV in immune-suppressed patients are heterogeneous with respect to IL-6 requirements for proliferation. An antitumoral effect in some of them can be achieved by neutralizing the IL-6-dependent proliferative loop.

Animals↗

PubMed1993

Two functionally different follicular dendritic cells in secondary lymphoid follicles of mouse spleen, as revealed by CR1/2 and FcR gamma II-mediated immune-complex trapping.

The capacity to trap immune complexes (IC) was examined using purified peroxidase-antiperoxidase IgG on frozen sections of mouse spleen. In the absence of serum, binding of IC was confined to macrophages in the red pulp. However, when IC were applied in the presence of fresh mouse serum as a source of complement, trapping occurred on follicular dendritic cells (FDC) in the primary follicles. Trapping was specifically inhibited with monoclonal antibodies against complement receptor type 1 (CR1) (8C12) and CR 1/2 (7G6), but not with anti-CR3 (Mac-1). The binding mechanism of IC in the secondary follicles of animals immunized with sheep red blood cells differed from that observed in unimmunized mice. Here, trapping occurred both in the absence and presence of fresh mouse serum. In the absence of fresh mouse serum, trapping on FDC was mediated by FcR gamma II, as demonstrated by blocking with monoclonal antibody 2.4G2. FcR gamma II-mediated trapping was only observed on a relatively small proportion of FDC that was located in the light zone of the secondary follicles, while complement receptor-mediated IC trapping was observed in more expanding areas, including dark zone and corona. These results show that both complement receptor as well as Fc receptor can function in the binding of IC to FDC. They also provide evidence for the existence of functionally different FDC populations in the secondary lymphoid follicles of mouse spleen.

Animals↗

PubMed1993

Characterization of the EBV/C3d receptor on the human Jurkat T cell line: evidence for a novel transcript.

EBV is a human herpes virus that causes mononucleosis and is associated with various tumors. EBV infects cells via the CR2 that was previously thought to be expressed only on the surface of B cells and certain epithelial cells. Recent findings in our laboratory and those of others, however, have shown that the EBV receptor is also present on T cells. Our study shows that Jurkat human T cells have a molecule that reacts with both anti-CR2 antibodies and the third component of complement, C3. Furthermore, the data indicate that this molecule binds EBV detected by incubation with biotin-conjugated virus and streptavidin phycoerythrin. Viral binding is specific, as it is inhibited by nonconjugated virus, with anti-CR2 antibodies, and with an antibody reactive with the glycoprotein (gp350) that EBV uses to bind CR2. In addition, EBV variably infects Jurkat cells as demonstrated by the presence of transcripts of Epstein Barr nuclear Ag (EBNA-1) using the polymerase chain reaction. Immunoprecipitation experiments with anti-CR2 antibodies and SDS-PAGE analysis reveal a protein with an apparent molecular mass of 155 kDa which is higher than the one seen in B cells. The size of this molecule is reduced to 119 kDa upon endoglycosidase F treatment. Northern blot analysis of Jurkat poly(A)+ RNA shows a transcript of 4.7 kb upon probing with the B cell CR2 cDNA. This size is consistent with that of B cell CR2 mRNA. Two cDNA clones were identified upon screening of a Jurkat cell cDNA library with the B cell CR2 cDNA. One of the clones possesses an identical nucleotide sequence to the one corresponding to B cell CR2, whereas the other represents a differentially spliced transcript which lacks the exon 8b of B cell CR2. Analysis of Jurkat and Raji mRNA by PCR demonstrated the presence of this novel splice variant in both cell lines.

Amino Acid Sequence↗

PubMed1996

EBV induces proliferation of immature human thymocytes in an IL-2-mediated response.

The receptor for EBV, CD21 is expressed on a population of immature human thymocytes and facilitates infection of these cells by EBV. Thymocytes infected by EBV become responsive to exogenous rIL-2- or CD2-mediated stimulation in vitro. To address whether such costimulation may be provided by thymic presenting cells and to study the cellular effects of EBV infection, the present work utilizes thymocyte cultures containing autologous thymic presenting cells. In the presence of these presenting cells, EBV induces proliferation of thymocytes. EBV infection promotes the formation of adhesions between two populations of cells in an APC responder fashion, and separation of these two populations abrogates the proliferative response to EBV. The response is mediated by IL-2 because Ab blocking of the IL-2R inhibits proliferation as does cyclosporin A. EBV promotes an expansion in the number of CD4+8+ thymocytes, and the proliferating population is vulnerable to TCR/CD3-generated signals, indicating that the responding cells are phenotypically and functionally immature. Finally, addition of exogenous IL-2 to EBV-exposed thymocytes promotes a second wave of proliferation. Phenotypic characterization of the EBV-induced, IL-2-responding cells shows them to express reduced levels of CD1 and a transitional CD4(high)8(low) phenotype. These data characterize the cellular response to EBV infection in thymocytes and may offer insight into EBV-associated T lineage malignancies and autoimmune disorders.

Antibodies, Blocking↗