Jose Vingerhoed - Academia.edu (original) (raw)
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Papers by Jose Vingerhoed
Tropical and geographical medicine, 1985
Title Decreasing sensitivity to RANTES (regulated on activation, normally T cell-expressed and-se... more Title Decreasing sensitivity to RANTES (regulated on activation, normally T cell-expressed and-secreted) neutralization of CC chemokine receptor 5-using, non-syncytium-inducing virus variants in the course of human immunodeficiency virus type 1 infection
Zeitschrift f�r Parasitenkunde Parasitology Research, 1985
Infective hookworm larvae of Ancylostoma caninum showed chemotaxis on agar plates in a dog serum ... more Infective hookworm larvae of Ancylostoma caninum showed chemotaxis on agar plates in a dog serum gradient. This chemotactic behaviour remain unaltered using an ultrafiltrated serum fraction with a molecular weight less than 500. Gelfiltration of this ultrafiltrated fraction revealed a factor with a molecular weight of 480 causing chemotaxis. The chemotactic activity of the factor was destroyed after a pronase treatment. We conclude that the factor could be a polypeptide.
Transplant Immunology, 2003
Previously, we established a murine model, that involves the engraftment of fully allogeneic T ce... more Previously, we established a murine model, that involves the engraftment of fully allogeneic T cell depleted donor bone marrow cells in sublethally irradiated and single dose anti-CD3 treated recipient mice. These mice developed permanent stable multilineage mixed chimerism and donor-specific tolerance without graft-versus-host disease. Recently, we have shown that donor-specific tolerance is not induced andyor maintained by clonal anergy, neither by a Th1yTh2 shift, nor by suppressor or other regulatory processes. In the present study, we investigated whether clonal deletion plays a role in tolerance induction in our model. We studied the kinetics of TCRVb8 T cells in BALByc (H-2L)™dm2 (H-2L) chimeras, in which combination of mouse q dq dy strains TCRVb8 predominates the anti-donor response. We found that TCRVb8 T cells were specifically deleted. To our q surprise, this deletion was also found in mixed chimeras, thymectomized prior to the conditioning regimen. We conclude that clonal deletion plays a role in the establishment and maintenance of donor-specific tolerance, and that the thymus is not required for this process. In addition, confocal laser-scanning microscopy clearly showed the presence of abundant amounts of donor T cells and some donor antigen presenting cells in the small intestine in thymectomized chimeras and not in other organs, suggesting that T cell selection might take place in this organ in the absence of the thymus.
Journal of Virology, 2001
In peripheral blood mononuclear cells, syncytium-inducing (SI) human immunodeficiency virus type ... more In peripheral blood mononuclear cells, syncytium-inducing (SI) human immunodeficiency virus type 1 (HIV-1) infected and depleted all CD4 + T cells, including naive T cells. Non-SI HIV-1 infected and depleted only the CCR5-expressing T-cell subset. This may explain the accelerated CD4 cell loss after SI conversion in vivo.
The Journal of Infectious Diseases, 2003
The presence of only non-syncytium-inducing b-chemokine receptor 5-restricted (R5/NSI) human immu... more The presence of only non-syncytium-inducing b-chemokine receptor 5-restricted (R5/NSI) human immunodeficiency virus type 1 (HIV-1) in an infected individual has been associated with long-term asymptomatic survival. However, the majority of R5/NSI HIV-1-infected individuals do progress to AIDS. Here, we compared the replicative capacity and cytopathicity of R5/NSI HIV-1 variants that were isolated early and late in the clinical course from 7 long-term asymptomatic individuals and 7 individuals with progressive HIV-1 infection. R5/NSI HIV-1 cytopathicity in vitro directly correlated with in vitro replication. HIV-1 variants obtained early and late during long-term asymptomatic HIV infection from the same individual were equally cytopathic. In contrast, HIV-1 variants obtained during late-stage progressive HIV infection were more cytopathic than viruses obtained early in infection from the same individuals. Our data indicate that the cytopathicity of HIV-1 variants may increase with progression to disease. The asymptomatic phase of infection with human immunodeficiency virus type 1 (HIV-1) is dominated by macrophage-tropic non-syncytium-inducing (NSI) HIV-1 variants that use CD4 and chemokine receptor CCR5 for entry in their target cells [1-5]. In 50% of HIV-1-infected individuals, disease progression is associated with the emergence of syncytium-inducing (SI) HIV-1
Human Immunology, 1991
Previously we have reported on the high degree of variation in the frequency of HLA-specific cyto... more Previously we have reported on the high degree of variation in the frequency of HLA-specific cytotoxicTlymphocyteprecursors (CTLpf). Our results confirmed the high values of CTLpf in general, but pointed to the observation that low or undetectable CTLpf against HLA class I antigens were found in the majority of healthy individuals, independently of their HLA phenotype. Identification of holes in the T-cell repertoire for class I antigens may be relevant for clinical transplantation, especially for hone marrow transplantation from unrelated donors. In order to determine the influence of genetic and environmental factors on the allorcactive CTL repertoire we compared CTLpf against various HLA antigens of s;.bling and monozygotic twin pairs from 9 families. In 8 of 15 of HLA-identical sibling pairs and in 8 of 12 HLA nonidentical sibling pairs significantly different CTLpf were found against certain HLA antigens. The antigens involved vary among the various pairs. In contrast, no such differences were found in the CTLpf of 5 monozygotic twin pairs. These data suggest that hereditary non-MHC factors have an important role in the generation of the functional alloreactive CTL repertoire.
Clinical Immunology, 2004
Studies in humans have provided evidence that CD8 + T cells exhibit distinct phenotypical and fun... more Studies in humans have provided evidence that CD8 + T cells exhibit distinct phenotypical and functional properties dependent on virus specificity. It is not known how these T-cell phenotypes develop over the course of infection. Dynamics and properties of T cells specific for human immunodeficiency virus (HIV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV) in HIV infection were investigated in relation to viral load. In rapid progressors, HIV-specific CD8 + T cells were less differentiated early in infection and did not develop a more differentiated phenotype. In slow progressors, perforin expression of HIV-specific CD8 + T cells slightly increased over time. HIV and EBV loads were detectable in all individuals, while CMV load could not be detected. Thus, in individuals with progressive HIV infection, HIVspecific T cells are less differentiated already early in infection. This apparent block in differentiation may be partly caused by chronic viremia or lack of CD4 + T-cell help.
AIDS, 2003
Background: A polymorphism at position À589 in the interleukin 4 (IL-4) promoter region was recen... more Background: A polymorphism at position À589 in the interleukin 4 (IL-4) promoter region was recently described as being associated with the presence of syncytiuminducing CXCR4 using (X4) HIV-1 variants. Objective: To study the IL-4 promoter polymorphism À589T in relation to HIV-1 disease progression and acquisition of X4 HIV-1 variants. Design and methods: Retrospective longitudinal study among 342 HIV-1-infected homosexual men who participated in the Amsterdam Cohort study. Polymerase chain reaction was used in combination with restriction analysis to identify IL-4 promoter genotypes.
Human Immunology, 1990
The following observations were made." (I) CTLpf against the same HLA antigen 1,ary among differe... more The following observations were made." (I) CTLpf against the same HLA antigen 1,ary among different responders; (2) CTLpf of one responder against various HLA antigens may be different; (3) "narrow" responders produce cytotoxic T lymphocytes that recognize only the private (stimulator) alloantigen, while "broad" responders produce mainly broadly cross-reactive cytotoxic T lymphocytes with public specificity. Split-well analysis shows that very few cytotoxic T lymphocytes of "broad" responders recognize the private alloantigen only. These individual variations are not dependent on the HLA phenotype, because they also occurred in unrelated HLA-identical responders stimulated against the same mismatched stimulator cells.
Scandinavian Journal of Rheumatology, 1990
HLA-B2703, a mutation of HLA-B2705, is characterized by a Tyr-to-His substitution at position 59 ... more HLA-B2703, a mutation of HLA-B2705, is characterized by a Tyr-to-His substitution at position 59 in the alpha 1 domain of the class-I heavy chain. So far, the HLA-B2703 subtype was found only in two Black individuals and it is the first polymorphism at position 59 of MHC class-I molecules. We have examined whether the single amino-acid substitution at position 59 results in an alloantigenic determinant and HLA-restriction element, and whether HLA-B2703 functionally differs from HLA-B2705. In vitro, HLA-B2703-positive lymphocytes were not stimulated by HLA-B2705-positive cells. Nevertheless, HLA-B2703 was recognized as an alloantigen. HLA-B2702-anti-HLA-B2705 CTL lysed HLA-B2703-positive cells less efficiently than HLA-B2705-positive cells. In addition, anti-HLA-B27 antibodies were found that lysed HLA-B2705 but not HLA-B2703 positive cells. Also, CTL clones have been described that can distinguish HLA-B2703 from HLA-B2705 (1). However, the HLA-B2703 subtype did not function as a private virus restriction element. HLA-B2705-restricted influenza virus-specific CTL also recognized HLA-B2703-positive virus-infected cells, and vice versa. Thus, the HLA-B2703 mutation represents an example of a class-I antigen without specific significance for the recognition of viral peptides.
Transplantation Proceedings, 2001
Clinical Chemistry and Laboratory Medicine, 2000
The Journal of Infectious Diseases, 2003
Tropical and geographical medicine, 1985
Title Decreasing sensitivity to RANTES (regulated on activation, normally T cell-expressed and-se... more Title Decreasing sensitivity to RANTES (regulated on activation, normally T cell-expressed and-secreted) neutralization of CC chemokine receptor 5-using, non-syncytium-inducing virus variants in the course of human immunodeficiency virus type 1 infection
Zeitschrift f�r Parasitenkunde Parasitology Research, 1985
Infective hookworm larvae of Ancylostoma caninum showed chemotaxis on agar plates in a dog serum ... more Infective hookworm larvae of Ancylostoma caninum showed chemotaxis on agar plates in a dog serum gradient. This chemotactic behaviour remain unaltered using an ultrafiltrated serum fraction with a molecular weight less than 500. Gelfiltration of this ultrafiltrated fraction revealed a factor with a molecular weight of 480 causing chemotaxis. The chemotactic activity of the factor was destroyed after a pronase treatment. We conclude that the factor could be a polypeptide.
Transplant Immunology, 2003
Previously, we established a murine model, that involves the engraftment of fully allogeneic T ce... more Previously, we established a murine model, that involves the engraftment of fully allogeneic T cell depleted donor bone marrow cells in sublethally irradiated and single dose anti-CD3 treated recipient mice. These mice developed permanent stable multilineage mixed chimerism and donor-specific tolerance without graft-versus-host disease. Recently, we have shown that donor-specific tolerance is not induced andyor maintained by clonal anergy, neither by a Th1yTh2 shift, nor by suppressor or other regulatory processes. In the present study, we investigated whether clonal deletion plays a role in tolerance induction in our model. We studied the kinetics of TCRVb8 T cells in BALByc (H-2L)™dm2 (H-2L) chimeras, in which combination of mouse q dq dy strains TCRVb8 predominates the anti-donor response. We found that TCRVb8 T cells were specifically deleted. To our q surprise, this deletion was also found in mixed chimeras, thymectomized prior to the conditioning regimen. We conclude that clonal deletion plays a role in the establishment and maintenance of donor-specific tolerance, and that the thymus is not required for this process. In addition, confocal laser-scanning microscopy clearly showed the presence of abundant amounts of donor T cells and some donor antigen presenting cells in the small intestine in thymectomized chimeras and not in other organs, suggesting that T cell selection might take place in this organ in the absence of the thymus.
Journal of Virology, 2001
In peripheral blood mononuclear cells, syncytium-inducing (SI) human immunodeficiency virus type ... more In peripheral blood mononuclear cells, syncytium-inducing (SI) human immunodeficiency virus type 1 (HIV-1) infected and depleted all CD4 + T cells, including naive T cells. Non-SI HIV-1 infected and depleted only the CCR5-expressing T-cell subset. This may explain the accelerated CD4 cell loss after SI conversion in vivo.
The Journal of Infectious Diseases, 2003
The presence of only non-syncytium-inducing b-chemokine receptor 5-restricted (R5/NSI) human immu... more The presence of only non-syncytium-inducing b-chemokine receptor 5-restricted (R5/NSI) human immunodeficiency virus type 1 (HIV-1) in an infected individual has been associated with long-term asymptomatic survival. However, the majority of R5/NSI HIV-1-infected individuals do progress to AIDS. Here, we compared the replicative capacity and cytopathicity of R5/NSI HIV-1 variants that were isolated early and late in the clinical course from 7 long-term asymptomatic individuals and 7 individuals with progressive HIV-1 infection. R5/NSI HIV-1 cytopathicity in vitro directly correlated with in vitro replication. HIV-1 variants obtained early and late during long-term asymptomatic HIV infection from the same individual were equally cytopathic. In contrast, HIV-1 variants obtained during late-stage progressive HIV infection were more cytopathic than viruses obtained early in infection from the same individuals. Our data indicate that the cytopathicity of HIV-1 variants may increase with progression to disease. The asymptomatic phase of infection with human immunodeficiency virus type 1 (HIV-1) is dominated by macrophage-tropic non-syncytium-inducing (NSI) HIV-1 variants that use CD4 and chemokine receptor CCR5 for entry in their target cells [1-5]. In 50% of HIV-1-infected individuals, disease progression is associated with the emergence of syncytium-inducing (SI) HIV-1
Human Immunology, 1991
Previously we have reported on the high degree of variation in the frequency of HLA-specific cyto... more Previously we have reported on the high degree of variation in the frequency of HLA-specific cytotoxicTlymphocyteprecursors (CTLpf). Our results confirmed the high values of CTLpf in general, but pointed to the observation that low or undetectable CTLpf against HLA class I antigens were found in the majority of healthy individuals, independently of their HLA phenotype. Identification of holes in the T-cell repertoire for class I antigens may be relevant for clinical transplantation, especially for hone marrow transplantation from unrelated donors. In order to determine the influence of genetic and environmental factors on the allorcactive CTL repertoire we compared CTLpf against various HLA antigens of s;.bling and monozygotic twin pairs from 9 families. In 8 of 15 of HLA-identical sibling pairs and in 8 of 12 HLA nonidentical sibling pairs significantly different CTLpf were found against certain HLA antigens. The antigens involved vary among the various pairs. In contrast, no such differences were found in the CTLpf of 5 monozygotic twin pairs. These data suggest that hereditary non-MHC factors have an important role in the generation of the functional alloreactive CTL repertoire.
Clinical Immunology, 2004
Studies in humans have provided evidence that CD8 + T cells exhibit distinct phenotypical and fun... more Studies in humans have provided evidence that CD8 + T cells exhibit distinct phenotypical and functional properties dependent on virus specificity. It is not known how these T-cell phenotypes develop over the course of infection. Dynamics and properties of T cells specific for human immunodeficiency virus (HIV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV) in HIV infection were investigated in relation to viral load. In rapid progressors, HIV-specific CD8 + T cells were less differentiated early in infection and did not develop a more differentiated phenotype. In slow progressors, perforin expression of HIV-specific CD8 + T cells slightly increased over time. HIV and EBV loads were detectable in all individuals, while CMV load could not be detected. Thus, in individuals with progressive HIV infection, HIVspecific T cells are less differentiated already early in infection. This apparent block in differentiation may be partly caused by chronic viremia or lack of CD4 + T-cell help.
AIDS, 2003
Background: A polymorphism at position À589 in the interleukin 4 (IL-4) promoter region was recen... more Background: A polymorphism at position À589 in the interleukin 4 (IL-4) promoter region was recently described as being associated with the presence of syncytiuminducing CXCR4 using (X4) HIV-1 variants. Objective: To study the IL-4 promoter polymorphism À589T in relation to HIV-1 disease progression and acquisition of X4 HIV-1 variants. Design and methods: Retrospective longitudinal study among 342 HIV-1-infected homosexual men who participated in the Amsterdam Cohort study. Polymerase chain reaction was used in combination with restriction analysis to identify IL-4 promoter genotypes.
Human Immunology, 1990
The following observations were made." (I) CTLpf against the same HLA antigen 1,ary among differe... more The following observations were made." (I) CTLpf against the same HLA antigen 1,ary among different responders; (2) CTLpf of one responder against various HLA antigens may be different; (3) "narrow" responders produce cytotoxic T lymphocytes that recognize only the private (stimulator) alloantigen, while "broad" responders produce mainly broadly cross-reactive cytotoxic T lymphocytes with public specificity. Split-well analysis shows that very few cytotoxic T lymphocytes of "broad" responders recognize the private alloantigen only. These individual variations are not dependent on the HLA phenotype, because they also occurred in unrelated HLA-identical responders stimulated against the same mismatched stimulator cells.
Scandinavian Journal of Rheumatology, 1990
HLA-B2703, a mutation of HLA-B2705, is characterized by a Tyr-to-His substitution at position 59 ... more HLA-B2703, a mutation of HLA-B2705, is characterized by a Tyr-to-His substitution at position 59 in the alpha 1 domain of the class-I heavy chain. So far, the HLA-B2703 subtype was found only in two Black individuals and it is the first polymorphism at position 59 of MHC class-I molecules. We have examined whether the single amino-acid substitution at position 59 results in an alloantigenic determinant and HLA-restriction element, and whether HLA-B2703 functionally differs from HLA-B2705. In vitro, HLA-B2703-positive lymphocytes were not stimulated by HLA-B2705-positive cells. Nevertheless, HLA-B2703 was recognized as an alloantigen. HLA-B2702-anti-HLA-B2705 CTL lysed HLA-B2703-positive cells less efficiently than HLA-B2705-positive cells. In addition, anti-HLA-B27 antibodies were found that lysed HLA-B2705 but not HLA-B2703 positive cells. Also, CTL clones have been described that can distinguish HLA-B2703 from HLA-B2705 (1). However, the HLA-B2703 subtype did not function as a private virus restriction element. HLA-B2705-restricted influenza virus-specific CTL also recognized HLA-B2703-positive virus-infected cells, and vice versa. Thus, the HLA-B2703 mutation represents an example of a class-I antigen without specific significance for the recognition of viral peptides.
Transplantation Proceedings, 2001
Clinical Chemistry and Laboratory Medicine, 2000
The Journal of Infectious Diseases, 2003