Biomedical subjects

M de Boer

Publications and source records attributed to M de Boer.

At least 73 records · Page 4Linked to original sources

PubMed1995

FcR cross-linking on monocytes results in impaired T cell stimulatory capacity.

Presentation of antigen to T lymphocytes without the appropriate co-stimulatory signals results in a state of antigen-specific unresponsiveness. Despite the presumed importance of the B7-CD28 interaction for the initiation and maintenance of T cell-mediated immune responses, relatively few studies have addressed the regulation of B7 expression. We have studied the expression of the CD80 (B7-1) and B7-2 molecules on peripheral blood monocytes following different activation signals, and it was demonstrated that not only IFN-gamma, but also granulocyte macrophage colony stimulating factor can induce CD80 expression on monocytes. In addition, we found that cross-linking of FcR on monocytes strongly inhibits the up-regulation of CD80 and B7-2, with as a functional consequence that the capacity to function as antigen presenting cells (APC) and to stimulate T cell activation is severely impaired. When cultures were prepared in 96-well plates coated with human IgG, stimulation of T cells with allogeneic monocytes resulted only in modest T cell proliferation and no detectable IL-2 secretion as compared with untreated culture plates or plates coated with Fab fragments of human IgG. Under these conditions cross-linking of CD28 on the T cells with specific mAb completely reverted the inhibitory effect observed after culture on IgG-coated plates. Furthermore, FcR cross-linking on monocytes strongly inhibited the capacity of monocytes to induce a specific memory T cell response to viral, bacterial and fungal antigens, whereas the treatment did not impair the capacity of the T cells to respond to pokeweed mitogen, phytohemagglutinin and concanavalin A. We conclude that after FcR cross-linking, the impaired APC function is most likely due to the inability of monocytes to provide the essential co-stimulatory signals to the T cells via the B7-CD28/CTLA-4 interaction.

Antibodies, Monoclonal↗

PubMed1995

Accessory signalling by B7-1 for T cell activation induced by anti-CD2: evidence for IL-2-independent CTL generation and CsA-resistant cytokine production.

Resting T cells can be activated by selected pairs of anti-CD2 MoAb. Activation is dependent on the presence of accessory cells, which can be replaced by either anti-CD28, or by the combination of IL-1 beta and IL-6. The present study was undertaken to investigate accessory signalling by B7-1, the natural ligand of CD28, in this pathway of T cell activation. 3T6 mouse fibroblasts were transfected with human B7-1 and used as accessory cells in cultures of purified resting human T cells. In the presence of a stimulating pair of anti-CD2 MoAb, T cell proliferation, production of cytokines (IL-2, IL-4, IL-10, GM-CSF, IFN-gamma and TNF-alpha), and generation of cytotoxic T lymphocytes were all supported by B7-1(+) 3T6 cells but not by control 3T6 cells. Blocking studies with anti-IL-2 + anti-IL-2R MoAb revealed both IL-2-dependent and IL-2-independent CTL generation after B7-1-mediated costimulation. Moreover, a partial or complete resistance to inhibition with CsA was observed for IL-2 production and CTL generation respectively in the presence of the costimulatory signal derived from B7-1-CD28 interaction. Anti-CD2 MoAb with B7-1 costimulation could directly induce proliferation, IL-2 production and generation of CTL activity in highly purified CD8+ T cells without the help of CD4+ T cells. We conclude that CD28 ligation with the natural ligand B7-1 provides a strong accessory signal for CD4 and CD8 cell activation through CD2.

Adult↗

PubMed1995

The epidemiology of HIV and syphilis among male commercial sex workers in northern Thailand.

OBJECTIVE: To examine the prevalence and incidence of HIV and syphilis, and risk behaviors for these infections, among 1,172 male commercial sex workers (CSW) followed prospectively from 1989 to 1994 in Chiang Mai, northern Thailand. METHODS: Twice yearly visits were conducted by the Thai Ministry of Public Health at all cooperating gay bars and clubs (17 sites) in Chiang Mai City as part of a national HIV sentinel surveillance. Men and boys who agreed were followed prospectively. Sentinel visits included an interview, HIV pre-test counseling, HIV and syphilis serology, condom distribution, and referral for post-test counseling. Participation was voluntary, confidential, and individual HIV results were available only to participating subjects. A total of 219 CSW were seen at least twice, allowing for incidence estimates based on 100 person-years (PY). RESULTS: Median age of male CSW was 20 years. Median time of work as a CSW was 4 months. Most men (57.6%) described themselves as heterosexual. Median number of clients was 2.5 per week, and reported condom use with clients was low: 42% reported inconsistent or no condom use, while 58% reported always using condoms. Reactive Venereal Disease Research Laboratory results were 7.6%, overall, but showed a declining trend. HIV prevalence was 1.4% in June 1989, 13.9% in June 1990, and 20.1% in December 1993, and showed a significant increasing trend. There were 27 incident HIV infections in 227.3 PY of observation, for an overall incidence during the 4.5-year period of 11.9 per 100 PY (95% confidence interval, 7.42-16.38). CONCLUSION: Male CSW in northern Thailand are at high risk for HIV despite current prevention efforts. The majority are heterosexual, which may be an important epidemiologic link in the spread of HIV between male CSW users and heterosexual women in Thailand.

Adolescent↗

PubMed1994

Anaerobic degradation of halogenated benzoic acids by photoheterotrophic bacteria.

From light-exposed enrichment cultures containing benzoate and a mixture of chlorobenzoates, a pure culture was obtained able to grow with 3-chlorobenzoate (3-CBA) or 3-bromobenzoate (3-BrBA) as the sole growth substrate anaerobically in the light. The thus isolated organism is a photoheterotroph, designated isolate DCP3. It is preliminarily identified as a Rhodopseudomonas palustris strain. It differs from Rhodopseudomonas palustris WS17, the only other known photoheterotroph capable of using 3-CBA for growth, in its independence of benzoate for growth with 3-CBA and in its wider substrate range: if grown on 3-CBA, it can also use 2-CBA, 4-CBA or 3,5-CBA.

Anaerobiosis↗

PubMed1994

B7/CD28-dependent IL-5 production by human resting T cells is inhibited by IL-10.

We analyzed the effects of rIL-10 on IL-5 production by human resting T cells isolated from peripheral blood. Resting T cells of healthy individuals required activation for 48 h with either anti-CD3 mAb cross-linked on B7/CD32-transfected mouse fibroblasts or PMA in conjunction with anti-CD28 mAb for optimal IL-5 secretion. In each condition, IL-5 secretion measured by ELISA was inhibited in a dose-dependent manner by rIL-10, whereas IFN-gamma production was not suppressed. The inhibitory effect of rIL-10 on IL-5 synthesis induced by PMA and anti-CD28 mAb was also observed at the mRNA level. In contrast with its action on T cells costimulated by B7/CD28 signaling, rIL-10 did not block IL-5 secretion in response to PMA and A23187 calcium ionophore. The inhibition of IL-5 production by rIL-10 was not due to IL-2 deprivation because it was not modified by the addition of exogenous rIL-2. Moreover, cyclosporin A, which inhibited IL-2 more efficiently than rIL-10 in response to anti-CD3 mAb and B7/CD32 transfected fibroblasts, did not reduce and even enhanced IL-5 production. Finally, we analyzed the influence of endogenously produced IL-10 on IL-5 secretion by T cells stimulated by PMA and anti-CD28 mAb. Addition of a neutralizing anti-IL-10 mAb increased IL-5 release in this system, indicating that endogenous IL-10 controls IL-5 production. We conclude that both rIL-10 and endogenous IL-10 inhibit IL-5 production by T cells costimulated by B7/CD28 signaling.

Animals↗

PubMed1994

The combination of anti-B7 monoclonal antibody and cyclosporin A induces alloantigen-specific anergy during a primary mixed lymphocyte reaction.

Interaction of CD28/CTLA-4 on T cells with B7 on antigen-presenting cells constitutes an important costimulatory signal for T cells and is responsible for cyclosporin A-resistant interleukin 2 (IL-2) gene expression and potentially also for prevention of anergy induction after T cell receptor triggering. In this paper, we demonstrate that addition of a monoclonal antibody to B7, which blocks B7-CD28/CTLA-4 interaction, and of cyclosporin A together, but not separately, to a primary mixed lymphocyte reaction of freshly isolated human T cells towards a human B cell line, induces nonresponsiveness of alloantigen-specific cytotoxic T lymphocyte precursors, whereas reactivity to a third party stimulator is intact. Nonresponsiveness could be reversed by culture in IL-2, indicating that anergy, and not clonal deletion, is responsible for this phenomenon. Our finding opens important perspectives for the development of new therapeutic strategies in transplantation.

Antibodies, Monoclonal↗

PubMed1994

Autosomal recessive chronic granulomatous disease with absence of the 67-kD cytosolic NADPH oxidase component: identification of mutation and detection of carriers.

Chronic granulomatous disease (CGD) is characterized by the failure of phagocytic leukocytes to kill certain bacteria and fungi. This is caused by deficiencies in one of the components of NADPH oxidase, the enzyme in phagocytic leukocytes that generates superoxide. In a rare, autosomal recessive form of CGD, a 67-kD cytosolic component of NADPH oxidase (p67-phox) is missing. Until now, mutations in the gene coding for this protein have not been identified. We now report on a 10-year-old girl with lymph node and liver abscesses who was recognized as an A67(0) CGD patient by lack of NADPH oxidase activity in her granulocytes, a cytosolic defect in a cell-free oxidase system, and lack of immunoreactive material with an antiserum against the p67-phox protein. mRNA for this protein was present in normal amounts in her monocytes. This p67-phox mRNA was reverse-transcribed, and the coding region was amplified by polymerase chain reaction in six overlapping fragments and was sequenced. The patient appeared to be homozygous for a G-233-->A mutation, resulting in a nonconservative amino acid change (78Gly-->Glu). This mutation was also found in the genomic DNA of this patient but not in that of 38 normal donors. Both parents and a sister proved to be carriers of the disease, as deduced from the mutation in only one allele. The carrier state was also manifested by intermediate superoxide production by their intact granulocytes and in the cell-free system.

Amino Acid Sequence↗

PubMed1994

Synergy between cyclosporin A and a monoclonal antibody to B7 in blocking alloantigen-induced T-cell activation.

Costimulatory signals are absolutely required for T-cell activation after T-cell receptor/major histocompatibility complex-peptide interaction. So far, the best-known candidate essential costimulatory signal is mediated by interaction of CD28 on T cells with B7 on antigen-presenting cells. Using an allogeneic B7+ Epstein-Barr virus-transformed B-cell line as stimulator, we found that addition of a monoclonal antibody (MoAb) to B7 that efficiently blocks B7-CD28 interaction only partially inhibited proliferation and interleukin-2 (IL-2) production in primary and secondary mixed lymphocyte reactions (MLR), whereas the generation of cytotoxic T lymphocytes (CTL) was not affected. Inhibition of primary or secondary MLR-induced T-cell activation with cyclosporin A (CsA) at nontoxic concentrations also was never complete. However, the combination of CsA and anti-B7 MoAb B7-24 synergistically blocked allogeneic B cell-induced T-cell proliferation, IL-2 production, and CTL generation. These data suggest that the mere blockage of B7-CD28 interaction during allotransplantation will be insufficient to prevent rejection or graft-versus-host disease. However, low CsA concentrations, when combined with an agent blocking B7-CD28 interaction, can potentially achieve complete immunosuppression.

Abatacept↗

PubMed1994

Professional presentation of antigen by activated human T cells.

Activated human T cells express class II molecules, but their capacity to present soluble antigens and stimulate T cells has been repeatedly questioned. Two lines of evidence indicate that T cells may indeed function as professional antigen-presenting cells. First, T cells that have been recently activated can efficiently capture, process and present tetanus toxoid to class II-restricted T cell clones. This capacity correlates with the rate of class II synthesis. Second, activated T cell clones express high levels of B7, are powerful stimulators in mixed lymphocyte reactions, and their stimulatory capacity is inhibited by soluble CTLA4 or anti-B7 antibody. Furthermore, expression of B7 can be detected in vivo on T cells from biopsies of patients with liver disease. Presentation of soluble antigen by activated T cells may play a role in the amplification of the specific response, and possibly in immunopathological states.

Antigen-Presenting Cells↗

PubMed1994

Helper effector function of human T cells stimulated by anti-CD3 mAb can be enhanced by co-stimulatory signals and is partially dependent on CD40-CD40 ligand interaction.

In this study we have investigated whether anti-CD3-induced human T cell help for immunoglobulin production could be enhanced by co-stimulation of the T cells via other T cell surface molecules, and the contribution of CD40-CD40 ligand interaction to the execution of T helper effector function induced by these different stimulatory signals. In a system in which irradiated tonsillar T cells were stimulated with immobilized anti-CD3 monoclonal antibody (mAb), it was found that ligation of CD2 with a mitogenic pair of mAb considerably enhanced anti-CD3-induced T cell help for immunoglobulin production. Likewise, ligation of CD28 with mAb enhanced T helper activity, although to a lesser extent. Upon addition of anti-CD28 and anti-CD2 mAb together, an even higher immunoglobulin production was observed. This combination resulted in a four- to fivefold increase in immunoglobulin production as compared to cultures in which T cells were stimulated with anti-CD3 mAb alone. The effect of ligation with B7, the natural ligand of CD28, was studied in a system which utilizes the presentation of anti-CD3 mAb on human Fc gamma RII-expressing mouse fibroblasts which were co-transfected with human B7. It appeared that B7 could stimulate help for immunoglobulin production much more efficiently than ligation of CD28 with mAb did. Physical separation of B cells from T cells led to complete abrogation of immunoglobulin production. Blocking of CD40 with specific mAb, which have no intrinsic B cell stimulatory properties, or the CD40 ligand with a soluble CD40-human IgM fusion protein, resulted in dose-dependent, but only partial, inhibition of T cell-dependent immunoglobulin production with all modes of T cell activation tested. A clear correlation was found between the induction of CD40 ligand expression on the T cells by the different modes of co-stimulation and subsequent immunoglobulin production by the B cells. It is concluded that ligation of CD28 and/or CTLA-4, and of CD2 can generate co-stimulatory signals for T cell help for immunoglobulin production, which was found to be only partially dependent on the CD40-CD40 ligand interaction.

Animals↗

PubMed1994

Interleukin-10 inhibits B7 and intercellular adhesion molecule-1 expression on human monocytes.

There is evidence that interleukin -10(IL-10) interferes with the costimulatory properties of antigen-presenting cells and, thereby, inhibits their ability to induce T cell activation. To determine whether this effect might involve modulation of the expression of accessory molecules, we analyzed by flow cytometry the influence of human IL-10 on the basal expression of intercellular adhesion molecule 1 (ICAM-1) as well as on the interferon gamma (IFN-gamma)-induced up-regulation of ICAM-1 and B7 at the surface of human monocytes. IL-10 inhibited both the basal expression and the IFN-gamma-induced ICAM-1 up-regulation. IL-10 also reduced B7 up-regulation on IFN-gamma-stimulated monocytes. The inhibitory effect of IL-10 both on ICAM-1 and B7 expression was shown to be dose dependent. We conclude that the ability of IL-10 to decrease both ICAM-1 and B7 expression on monocytes might contribute to its immunosuppressive properties.

B7-1 Antigen↗

PubMed1994

Differences in responsiveness to CD3 stimulation between naive and memory CD4+ T cells cannot be overcome by CD28 costimulation.

Activation of naive CD4+ T cells is essential for the induction of primary immune responses. However, this subset is less responsive to signaling via T cell receptor/CD3 (TcR/CD3) complex than memory CD4+ cells. For mitogenic activation of T cells, in addition to triggering of the TcR/CD3 complex, costimulatory signals are required that can be generated by surface structures present on the antigen-presenting cells. We investigated here whether differences in responsiveness to TcR/CD3 stimulation of naive and memory cells can be overcome by the costimulatory pathway B7/CD28. Using a B7-dependent system we show that even in the presence of optimal CD28 costimulation, CD4+ naive cells still have more stringent TcR/CD3 activation requirements than memory cells. Furthermore, titration of the B7 signal revealed that for activation of naive CD4+ cells a higher level of cross-linking of CD28 molecules is required than for memory cells. Thus, our results show that at least two signals are required for activation of both CD4+ memory and naive cells, but that for activation of naive cells higher cross-linking of both CD3 and CD28 molecules is necessary.

Animals↗

PubMed1994

Interleukin-1 and B7/CD28 interaction regulate interleukin-6 production by human T cells.

Production of interleukin-6 (IL-6) by the Th2 subset of murine T cells supposedly contributes to regulation of humoral immunity. Little information exists on IL-6 production by human T cells. We examined the requirements for IL-6 production by purified human blood T cells, completely depleted of IL-6-producing monocyte-accessory cells. Immobilized anti-CD3 mAb alone (coated on the culture wells) was unable to induce IL-6 production, although it could induce production of IL-2 and TNF-alpha. Addition of rIL-1 beta as an accessory signal to anti-CD3-stimulated human T cells induced IL-6 mRNA expression and protein secretion, while IL-2, IL-4, GM-CSF, IFN-gamma, or TNF-alpha did not have any effect. In the presence of IL-1 beta, both CD4+ and CD8+ T cells were able to produce IL-6. We also demonstrated that phorbol 12-myristate 13-acetate (PMA) or triggering of the CD28 molecule is an effective helper signal for IL-6 production by anti-CD3-stimulated T cells. Efficient CD28 ligation was done either by anti-CD28 mAb or by binding to its natural ligand B7/BB1, presented on the 3T6 mouse fibroblast cell line coexpressing transfected human Fc gamma RII (CD32) (to immobilize anti-CD3) and B7/BB1. Finally, we found that combinations of IL-1 beta with anti-CD28 mAb or PMA with anti-CD28 mAb were highly synergistic helper signals for IL-6 production. We conclude that IL-6 production by T cells is not induced by T cell receptor triggering alone, but different intracellular signaling pathways activated by IL-1 beta, CD28 ligation, or PMA efficiently coinduce IL-6 production.

Adult↗

PubMed1994

Identification of allele-specific p22-phox mutations in a compound heterozygous patient with chronic granulomatous disease by mismatch PCR and restriction enzyme analysis.

A rare subgroup (approx. 5%) of all chronic granulomatous disease (CGD) patients suffers from mutations in the gene encoding the small p22-phox subunit of the flavocytochrome b558 heterodimer, the terminal redox component of the phagocyte NADPH oxidase. A male CGD patient with neutrophil granulocytes devoid of any spectrometrically detectable cytochrome b558 owing to autosomally inherited p22-phox deficiency (phenotype, A22-) is reported. The patient was identified as being compound heterozygous for two independent mutations of his p22-phox alleles. On the maternal allele a single base substitution (A186 to T) was found that predicts a nonconservative replacement of Glu 53 by Val. On his paternal p22-phox allele a G was found to be added to a G stretch between nucleotides G195 and G199 in the cDNA sequence. The resulting frame shift predicts an aberrant open reading frame, 16 amino acids longer than the normal p22-phox polypeptide. Genomic DNA was tested for the presence of the mutant allele by mismatch PCR (polymerase chain reaction). For this purpose, a single base mismatch was introduced at nucleotide position 189, leading to digestion of the normal allele by the restriction enzyme HinfI. The maternal allele was found to be present in 50% of the patient's DNA and in 50% of the DNA from his mother. The same mismatch PCR analysis with control DNA from 35 healthy individuals ruled out the possibility that the single base substitution (A186 to T) represents a common polymorphism. Inheritance of the second allelic mutation (G insertion) was verified by restriction enzyme analysis using BslI [CC(N)7GG] to digest PCR-amplified genomic DNA at the mutation site. PCR in combination with restriction enzyme analysis proved to be a powerful tool for verification of point mutations in the compound heterozygous CGD patient analyzed and may be used for prenatal diagnosis in this family.

Alleles↗

PubMed1994

A point mutation in gp91-phox of cytochrome b558 of the human NADPH oxidase leading to defective translocation of the cytosolic proteins p47-phox and p67-phox.

The superoxide-forming NADPH oxidase of human phagocytes is composed of membrane-bound and cytosolic proteins which, upon cell activation, assemble on the plasma membrane to form the active enzyme. Patients suffering from chronic granulomatous disease (CGD) are defective in one of the following components: p47-phox and p67-phox, residing in the cytosol of resting phagocytes, and gp91-phox and p22-phox, constituting the membrane-bound cytochrome b558. In an X-linked CGD patient we identified a novel missense mutation predicting an Asp-->Gly substitution at residue 500 of gp91-phox, associated with normal amounts of nonfunctional cytochrome b558 in the patient's neutrophils. In PMA-stimulated neutrophils and in a cell-free translocation assay with neutrophil membranes and cytosol, the association of the cytosolic proteins p47-phox and p67-phox with the membrane fraction of the patient was strongly disturbed. Furthermore, a synthetic peptide mimicking domain 491-504 of gp91-phox inhibited NADPH oxidase activity in the cell-free assay (IC50 about 10 microM), and the translocation of p47-phox and p67-phox in the cell-free translocation assay. We conclude that residue 500 of gp91-phox resides in a region critical for stable binding of p47-phox and p67-phox.

Amino Acid Sequence↗

PubMed1994

Safe handling of antineoplastic drugs. Results of a survey.

As research continues to highlight the risks involved in handling antineoplastic drugs, the health services are giving increased attention to safety measures. In order to establish what protective measures nursing staff employ and what they know about antineoplastic drugs, a survey was carried out in The Netherlands. The questions were based on the self-study modules by Dunne and the (American) Oncology Nursing Society. A total of 1,373 questionnaires were distributed in 10 hospitals. Of these, 824 were returned, which represents a response rate of 60%. Over two-thirds (68%) of the nursing staff reported that they were involved, on a daily or weekly basis, in caring for patients being treated with antineoplastic drugs. In the view of 94% of the nurses, protective measures are effective. While administering antineoplastic drugs, 91% of the respondents said that they wore gloves, 21% said that they wore a gown, 18% wore a mask, and 3% used goggles. While handling excreta, fewer nurses applied safety measures. Thirty-nine percent of the respondents knew that latex gloves offer a greater degree of protection than PVC gloves. It appeared that there was not one Dutch hospital whose guidelines for the safe handling of antineoplastic material were completely up-to-date and that nurses do not always follow the guidelines established.

Antineoplastic Agents↗

PubMed1994

Design and analysis of PCR primers for the amplification and cloning of human immunoglobulin Fab fragments.

We have developed PCR primers for the amplification and cloning of the genes encoding human antibody fragments. Two sets of primers were designed to amplify the coding sequence of the complete variable region and the first constant domain of immunoglobulin heavy chains. One set of primers was designed to amplify the coding sequence of complete kappa light chains. These three sets of primers were used in PCR amplifications with cDNA prepared from EBV transformed B cells as the template. The amplified fragments were cloned and their nucleotide sequences were determined. Analysis of the DNA sequences of such PCR generated antibody fragments suggested that our primer sets were able to amplify the major subsets of the heavy and light chain variable region genes. Comparison between the estimated frequency of the different subsets of heavy chain variable region genes and the distribution of our subclones further indicated that one set of our primers was able to proportionally amplify the subsets of the heavy chain family.

Amino Acid Sequence↗

PubMed1993

The B7/BB1 antigen is expressed by Reed-Sternberg cells of Hodgkin's disease and contributes to the stimulating capacity of Hodgkin's disease-derived cell lines.

The B7/BB1 molecule has recently been found to be expressed on professional antigen-presenting cells and to be the natural ligand for CD28 and CTLA-4 on T cells. On binding of B7/BB1, CD28 transduces a signal that synergizes with triggering of the T-cell antigen receptor, resulting in enhanced cytokine secretion. In view of the data supporting an antigen-presenting function of Reed-Sternberg cells, we evaluated the expression of B7/BB1 in lymph nodes affected by Hodgkin's disease. B7/BB1 was found to be strongly expressed by the Reed-Sternberg cells in all 47 cases of Hodgkin's disease studied. Moreover, Reed-Sternberg cells were frequently surrounded by CD28-expressing T cells. Evidence for a functional role of B7/BB1 on Reed-Sternberg cells was obtained by our findings that T-cell proliferation and interleukin-2 (IL-2) production in the primary allogenic mixed lymphocyte reaction (MLR), using the B7/BB1-expressing Hodgkin's disease-derived cell lines L428 and KM-H2 as stimulators, could be partially blocked by adding anti-B7 monoclonal antibody. B7/BB1 expression was also evaluated in a group of non-Hodgkin's lymphomas (n = 46). Whereas B7/BB1 was not expressed by the neoplastic cells of most non-Hodgkin's lymphomas, including T-cell-rich B-cell lymphoma (n = 11), it was present on the neoplastic cells of anaplastic large-cell lymphoma (Ki-1 lymphoma) (n = 5) and follicular lymphoma (n = 4). Our data provide further evidence for an accessory cell function of Reed-Sternberg cells. The accessory cell function of Reed-Sternberg cells might lead to pronounced T-cell activation in vivo, which might contribute to the Hodgkin's syndrome. In addition, our study indicates that B7/BB1 may be a useful marker for differentiating Hodgkin's disease from morphologically similar conditions such as T-cell-rich B-cell lymphoma.

Animals↗