The Experts below are selected from a list of 72 Experts worldwide ranked by ideXlab platform
Sven Bergström - One of the best experts on this subject based on the ideXlab platform.
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Relapsing fever Borrelia binds to neolacto glycans and mediates Rosetting of human Erythrocytes
Proceedings of the National Academy of Sciences of the United States of America, 2009Co-Authors: Betty P. Guo, Susann Teneberg, Robert Münch, Daiyo Terunuma, Ken Hatano, Koji Matsuoka, Jonas Ångström, Thomas Borén, Sven BergströmAbstract:A hallmark of acute relapsing fever borreliosis is severe bacteremia. Some Borrelia species, such as B. duttonii and B. crocidurae, associate with Erythrocytes and induce aggregation recognized as Erythrocyte Rosetting. Erythrocyte rosettes contribute to disease severity by increased tissue invasiveness (such as invasion of CNS and encephalitis), hemorrhaging, and reduced blood flow in affected microcapillaries. Here we report that relapsing fever Borrelia binds to neolacto (Galβ4GlcNAcβ3Galβ4Glcβ1)–carrying glycoconjugates that are present on human Erythrocytes. This interaction is of low affinity but is compensated for by the multivalency of neo-lacto-oligosaccharides on the Erythrocyte cell surface. Hence, the protein–carbohydrate interaction is dependent on multivalent neolacto-glycans to mediate binding.
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The spirochete Borrelia crocidurae causes Erythrocyte Rosetting during relapsing fever
Infection and immunity, 1998Co-Authors: Nils Burman, Alireza Shamaei-tousi, Sven BergströmAbstract:Several species of the genus Borrelia exhibit antigenic variation of variable major proteins on their surface during relapsing fever. We have investigated the African relapsing fever species Borrelia crocidurae during infections in mice and compared it with the thoroughly studied North American species Borrelia hermsii. A major difference between the two species is that B. crocidurae can bind and become completely covered with Erythrocytes. In addition, B. crocidurae causes a prolonged spirochetemia which coincides with a delayed appearance of antiborrelial antibodies. We show that the antibody response against an unrelated antigen is not delayed and that antibiotic treatment, which dissociates rosettes and inhibits the spirochetes, also leads to an early antibody response. Taken together, the Erythrocyte aggregation and prolonged spirochetemia hint at a new mode of immune evasion where Erythrocyte-covered spirochetes may avoid contact with the phagocytic cells and B cells of the immune system, thereby delaying the onset of a specific immune response.
F E Ward - One of the best experts on this subject based on the ideXlab platform.
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hematopoietic stem cell transplantation for the treatment of severe combined immunodeficiency
The New England Journal of Medicine, 1999Co-Authors: Rebecca H. Buckley, Sherrie E. Schiff, Richard I. Schiff, Louise M Markert, Larry W Williams, Joseph L Roberts, Laurie Myers, F E WardAbstract:Background Since 1968 it has been known that bone marrow transplantation can ameliorate severe combined immunodeficiency, but data on the long-term efficacy of this treatment are limited. We prospectively studied immunologic function in 89 consecutive infants with severe combined immunodeficiency who received hematopoietic stem-cell transplants at Duke University Medical Center between May 1982 and September 1998. Methods Serum immunoglobulin levels and lymphocyte phenotypes and function were assessed and genetic analyses performed according to standard methods. Bone marrow was depleted of T cells by agglutination with soybean lectin and by sheep-Erythrocyte Rosetting before transplantation. Results Seventy-seven of the infants received T-cell–depleted, HLA-haploidentical parental marrow, and 12 received HLA-identical marrow from a related donor; 3 of the recipients of haploidentical marrow also received placental-blood transplants from unrelated donors. Except for two patients who received placental bloo...
Liz Stevenson - One of the best experts on this subject based on the ideXlab platform.
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investigating the function of fc specific binding of igm to plasmodium falciparum Erythrocyte membrane protein 1 mediating Erythrocyte Rosetting
Cellular Microbiology, 2015Co-Authors: Liz Stevenson, Pie Huda, Anine Jeppesen, Erik Laursen, Alexandra J Rowe, Alister Craig, Werner StreicherAbstract:Acquired protection from Plasmodium falciparum malaria takes years to develop, probably reflecting the ability of the parasites to evade immunity. A recent example of this is the binding of the Fc region of IgM to VAR2CSA-type PfEMP1. This interferes with specific IgG recognition and phagocytosis of opsonized infected Erythrocytes (IEs) without compromising the placental IE adhesion mediated by this PfEMP1 type. IgM also binds via Fc to several other PfEMP1 proteins, where it has been proposed to facilitate Rosetting (binding of uninfected Erythrocytes to a central IE). To further dissect the functional role of Fc -mediated IgM binding to PfEMP1, we studied the PfEMP1 protein HB3VAR06, which mediates Rosetting and binds IgM. Binding of IgM to this PfEMP1 involved the Fc domains Cμ3-Cμ4 in IgM and the penultimate DBL domain (DBLζ2) at the C-terminus of HB3VAR06. However, IgM binding did not inhibit specific IgG labelling of HB3VAR06 or shield IgG-opsonized IEs from phagocytosis. Instead, IgM was required for Rosetting, and each pentameric IgM molecule could bind two HB3VAR06 molecules. Together, our data indicate that the primary function of Fc -mediated IgM binding in Rosetting is not to shield IE from specific IgG recognition and phagocytosis as in VAR2CSA-type PfEMP1. Rather, the function appears to be strengthening of IE-Erythrocyte interactions. In conclusion, our study provides new evidence on the molecular details and functional significance of Rosetting, a long-recognized marker of parasites that cause severe P. falciparum malaria.
Rebecca H. Buckley - One of the best experts on this subject based on the ideXlab platform.
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hematopoietic stem cell transplantation for the treatment of severe combined immunodeficiency
The New England Journal of Medicine, 1999Co-Authors: Rebecca H. Buckley, Sherrie E. Schiff, Richard I. Schiff, Louise M Markert, Larry W Williams, Joseph L Roberts, Laurie Myers, F E WardAbstract:Background Since 1968 it has been known that bone marrow transplantation can ameliorate severe combined immunodeficiency, but data on the long-term efficacy of this treatment are limited. We prospectively studied immunologic function in 89 consecutive infants with severe combined immunodeficiency who received hematopoietic stem-cell transplants at Duke University Medical Center between May 1982 and September 1998. Methods Serum immunoglobulin levels and lymphocyte phenotypes and function were assessed and genetic analyses performed according to standard methods. Bone marrow was depleted of T cells by agglutination with soybean lectin and by sheep-Erythrocyte Rosetting before transplantation. Results Seventy-seven of the infants received T-cell–depleted, HLA-haploidentical parental marrow, and 12 received HLA-identical marrow from a related donor; 3 of the recipients of haploidentical marrow also received placental-blood transplants from unrelated donors. Except for two patients who received placental bloo...
Werner Streicher - One of the best experts on this subject based on the ideXlab platform.
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investigating the function of fc specific binding of igm to plasmodium falciparum Erythrocyte membrane protein 1 mediating Erythrocyte Rosetting
Cellular Microbiology, 2015Co-Authors: Liz Stevenson, Pie Huda, Anine Jeppesen, Erik Laursen, Alexandra J Rowe, Alister Craig, Werner StreicherAbstract:Acquired protection from Plasmodium falciparum malaria takes years to develop, probably reflecting the ability of the parasites to evade immunity. A recent example of this is the binding of the Fc region of IgM to VAR2CSA-type PfEMP1. This interferes with specific IgG recognition and phagocytosis of opsonized infected Erythrocytes (IEs) without compromising the placental IE adhesion mediated by this PfEMP1 type. IgM also binds via Fc to several other PfEMP1 proteins, where it has been proposed to facilitate Rosetting (binding of uninfected Erythrocytes to a central IE). To further dissect the functional role of Fc -mediated IgM binding to PfEMP1, we studied the PfEMP1 protein HB3VAR06, which mediates Rosetting and binds IgM. Binding of IgM to this PfEMP1 involved the Fc domains Cμ3-Cμ4 in IgM and the penultimate DBL domain (DBLζ2) at the C-terminus of HB3VAR06. However, IgM binding did not inhibit specific IgG labelling of HB3VAR06 or shield IgG-opsonized IEs from phagocytosis. Instead, IgM was required for Rosetting, and each pentameric IgM molecule could bind two HB3VAR06 molecules. Together, our data indicate that the primary function of Fc -mediated IgM binding in Rosetting is not to shield IE from specific IgG recognition and phagocytosis as in VAR2CSA-type PfEMP1. Rather, the function appears to be strengthening of IE-Erythrocyte interactions. In conclusion, our study provides new evidence on the molecular details and functional significance of Rosetting, a long-recognized marker of parasites that cause severe P. falciparum malaria.