The Experts below are selected from a list of 13806 Experts worldwide ranked by ideXlab platform
Menno C Van Zelm - One of the best experts on this subject based on the ideXlab platform.
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aBsence of surface igd does not impair <B>NaiveB> B Cell homeostasis or memory B Cell formation in ighd haploinsufficient humans
Journal of Immunology, 2018Co-Authors: Jana Nechvatalova, Sophinus J W Bartol, Zita Chovancova, Louis Boon, Marcela Vlkova, Menno C Van ZelmAbstract:Surface IgD is coexpressed with IgM on <B>NaiveB> mature B Cells. Still, the role of surface IgD remains enigmatic even 50 y after its initial discovery. In this study, we examined the in vivo role of surface IgD in human B Cell homeostasis and AB responses in four individuals with heterozygous nonsense mutations in IGHD All IGHD heterozygous individuals had normal numBers of B Cells and serum Igs and did not show signs of immunodeficiency or immune dysregulation. IgD+ and IgD- <B>NaiveB> mature B Cells were present in equal numBers and showed similar immunophenotypes, except for decreased expression of CD79B in the IgD- suBset. Furthermore, Both IgD+ and IgD- <B>NaiveB> mature B Cells had normal replication histories and similar capacities to differentiate into plasma Cells upon in vitro stimulation, and Ig class-switched memory B Cells showed similar levels of somatic hypermutations. Thus, human B Cells lacking IgD expression develop normally and generate immunological memory in vivo, suggesting that surface IgD might function more restrictedly in regulating of B Cell activation to specific antigenic structures.
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aBsence of surface igd does not impair <B>NaiveB> B Cell homeostasis and memory B Cell formation in humans
bioRxiv, 2018Co-Authors: Jana Nechvatalova, Sophinus J W Bartol, Zita Chovancova, Louis Boon, Marcela Vlkova, Menno C Van ZelmAbstract:Surface immunogloBulin D (IgD) is co-expressed with IgM on <B>NaiveB> mature B Cells. Still, the role of surface IgD remains enigmatic even 50 years after its initial discovery. We here examined the in vivo role of surface IgD in human B-Cell homeostasis and antiBody responses in four individuals with heterozygous nonsense mutations in IGHD. All IGHD heterozygous individuals had normal numBers of B Cells and serum immunogloBulins, and did not show signs of immunodeficiency or immune dysregulation. IgD+ and IgD- <B>NaiveB> mature B Cells were present in equal numBers and showed similar immunophenotypes, except for decreased expression of CD79B in the IgD- suBset. Furthermore, Both IgD+ and IgD- <B>NaiveB> mature B Cells had normal replication histories, similar capacities to differentiate into plasma Cells upon in vitro stimulation, and Ig switched memory B Cells showed similar levels of somatic hypermutations. Thus human B Cells lacking IgD expression develop normally and generate immunological memory in vivo, suggesting that surface IgD might function more restricted in regulating of B-Cell activation to specific antigenic structures.
I Bates - One of the best experts on this subject based on the ideXlab platform.
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vh gene sequences from a novel tropical splenic lymphoma reveal a <B>NaiveB> B Cell as the Cell of origin
British Journal of Haematology, 1999Co-Authors: Andrew R Thompsett, George Beduaddo, Freda K Stevenson, I BatesAbstract:The prevalence of malaria and other infections in tropical Africa provides a setting for the emergence of B-Cell tumours distinct from that in Western countries. Attempts to draw comparisons with Western lymphomas have led to difficulties, with so-called African chronic lymphocytic leukaemia (CLL) having a different pattern of incidence from Western CLL. Splenomegaly is common in African CLL, and this has posed diagnostic proBlems in differentiating the tumour from malaria-associated hyper-reactive malarial splenomegaly (HMS). One feature of the splenomegalic form of African CLL is that the tumour Cells often possess short But fine cytoplasmic projections reminiscent of those oBserved in Western splenic lymphoma with villous lymphocytes (SLVL). Analysis of Ig VH genes Both facilitates discrimination Between clonal B-Cell tumours and HMS, and reveals the differentiation status of the Cell of origin. This study indicated that VH genes of nine cases of clonal splenic B-Cell tumours with villous lymphocytes from Ghana were relatively unmutated, consistent with an origin from a <B>NaiveB> B Cell. These features differ from SLVL which arises from a post-follicular antigen-selected B Cell. One possiBility is that these splenic B-Cell tumours derive from a splenic T-independent B Cell, with malaria infection as a potential influence.
Scott F. Sieg - One of the best experts on this subject based on the ideXlab platform.
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impaired <B>NaiveB> and memory B Cell responsiveness to tlr9 stimulation in human immunodeficiency virus infection
Journal of Virology, 2008Co-Authors: Wei Jiang, Michael M. Lederman, Clifford V. Harding, Benigno Rodriguez, Richard J. Mohner, Todd M Nedrich, Scott F. SiegAbstract:Toll-like receptor 9 (TLR9) agonists such as unmethylated Bacterial CpG DNAs activate B lymphocytes directly, potentially influencing their function and homeostasis. To assess B-Cell responsiveness to TLR9 agonists in human immunodeficiency virus (HIV) disease, we examined the aBility of <B>NaiveB> and memory B Cells to proliferation and to increase surface expression of CD80 in response to CpG oligonucleotides (ODN). CpG ODN induced expression of CD80 similarly in B Cells from HIV-infected persons and from healthy controls. In contrast, proliferation responses to CpG ODN were markedly impaired in Both <B>NaiveB> and memory B-Cell suBsets from HIV-infected persons. <B>NaiveB> B-Cell proliferation defects were related to plasma HIV RNA and, among memory B Cells, to the frequencies of CD21-negative Cells. Importantly, TLR9 mRNA levels were significantly diminished in freshly prepared <B>NaiveB> B Cells and especially so in memory B Cells from HIV-positive viremic donors, suggesting a possiBle underlying mechanism for the oBserved functional impairments. Dose-response studies indicated that optimal induction of CD80 expression was achieved with much lower concentrations of CpG ODN than optimal induction of proliferation. We propose that the relatively low threshold of activation that is required for CD80 induction By CpG ODN might explain the preservation of this response in B Cells from HIV-infected persons despite diminished TLR9 expression. Impaired responsiveness to TLR9 agonists may contriBute to defects in humoral immunity in HIV infection.
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TLR9 stimulation drives naïve B Cells to proliferate and to attain enhanced antigen presenting function.
European journal of immunology, 2007Co-Authors: Wei Jiang, Michael M. Lederman, Clifford V. Harding, Benigno Rodriguez, Richard J. Mohner, Scott F. SiegAbstract:Mechanisms that regulate <B>NaiveB> B Cell proliferation and function are incompletely defined. In this study, we test the hypothesis that <B>NaiveB> B Cell expansion, survival and aBility to present antigen to T lymphocytes can Be directly modulated By Toll-like receptor (TLR) agonists. In the aBsence of B Cell receptor stimulation, CpG oligonucleotide, a TLR9 agonist, was particularly efficient in inducing <B>NaiveB> B Cell proliferation and survival. Although the expanded <B>NaiveB> B Cells did not mature into CD27+ or IgG+ memory B Cells, these Cells did differentiate into IgM-secreting Cells with increased surface expression of HLA-DR, CD40 and CD80. This was associated with an increased potential for these B Cells to activate allogeneic T Cells. We propose that the activation and expansion of <B>NaiveB> B Cells induced By TLR9 agonists could enhance the potential of these Cells to interact with cognate antigens and facilitate Cell-mediated immune responses.
David A. Thorley-lawson - One of the best experts on this subject based on the ideXlab platform.
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The Mechanism of Epstein-Barr Virus Persistence in Vivo and its Relationship to the Origins of EBV Associated Lymphoma
Retrovirology, 2005Co-Authors: David A. Thorley-lawsonAbstract:Epstein-Barr virus persists latently within resting memory B lymphocytes. To gain access to this compartment the virus first infects and activates a <B>NaiveB> B Cell and then drives it to differentiate into a resting memory B Cell. To achieve this the virus uses four different viral latent gene transcription programs which are also expressed in EBV associated lymphomas e.g. the growth program in immunoBlastic lymphoma, the default program in Hodgkin's disease and the EBNA1 only program in Burkitt's lymphoma. This suggests:
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Cells Expressing the Epstein-Barr Virus Growth Program Are Present in and Restricted to the <B>NaiveB> B-Cell SuBset of Healthy Tonsils
Journal of virology, 2000Co-Authors: Alexandra M. Joseph, Gregory J. Babcock, David A. Thorley-lawsonAbstract:In this paper we demonstrate, for the first time, that Epstein-Barr virus (EBV)-infected Cells expressing the lymphoBlastoid growth program are present in healthy carriers of the virus. Previously we oBserved that latently infected <B>NaiveB> B Cells are present in tonsils only when viral replication is detected, suggesting that these may represent newly infected B Cells. We have tested this idea By performing a reverse transcription-PCR analysis for the expression of latent genes (EBNA2 and the EBNA3s) that are characteristically expressed only By newly infected Cells expressing the growth latency program. EBNA2 expression is regularly detected in purified <B>NaiveB> (IgD+) tonsillar B Cells (13 of 16 tonsils tested) But was never found in the IgD− population (0 of 16). More detailed analysis revealed that the mRNAs for the latent genes EBNA1 (3 of 3 tonsils tested), EBNA3a (3 of 5), EBNA3B (3 of 5), EBNA3c (3 of 5), LMP1 (6 of 6), and LMP2 (5 of 6) were also present in the IgD+ population, But the EBNA1Q-K transcript, characteristic of nonlymphoBlastoid forms of latency, was never detected (0 of 6). Finally, we demonstrate that the latently infected <B>NaiveB> (IgD+) Cells express CD80 (B7.1), a marker characteristically expressed on activated <B>NaiveB> lymphoBlasts But aBsent from resting <B>NaiveB> B Cells. The infected <B>NaiveB> (IgD+) population in the tonsil therefore has the viral and Cellular phenotype of a B-Cell directly infected with EBV—an activated lymphoBlast expressing the growth program.
Wei Jiang - One of the best experts on this subject based on the ideXlab platform.
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impaired <B>NaiveB> and memory B Cell responsiveness to tlr9 stimulation in human immunodeficiency virus infection
Journal of Virology, 2008Co-Authors: Wei Jiang, Michael M. Lederman, Clifford V. Harding, Benigno Rodriguez, Richard J. Mohner, Todd M Nedrich, Scott F. SiegAbstract:Toll-like receptor 9 (TLR9) agonists such as unmethylated Bacterial CpG DNAs activate B lymphocytes directly, potentially influencing their function and homeostasis. To assess B-Cell responsiveness to TLR9 agonists in human immunodeficiency virus (HIV) disease, we examined the aBility of <B>NaiveB> and memory B Cells to proliferation and to increase surface expression of CD80 in response to CpG oligonucleotides (ODN). CpG ODN induced expression of CD80 similarly in B Cells from HIV-infected persons and from healthy controls. In contrast, proliferation responses to CpG ODN were markedly impaired in Both <B>NaiveB> and memory B-Cell suBsets from HIV-infected persons. <B>NaiveB> B-Cell proliferation defects were related to plasma HIV RNA and, among memory B Cells, to the frequencies of CD21-negative Cells. Importantly, TLR9 mRNA levels were significantly diminished in freshly prepared <B>NaiveB> B Cells and especially so in memory B Cells from HIV-positive viremic donors, suggesting a possiBle underlying mechanism for the oBserved functional impairments. Dose-response studies indicated that optimal induction of CD80 expression was achieved with much lower concentrations of CpG ODN than optimal induction of proliferation. We propose that the relatively low threshold of activation that is required for CD80 induction By CpG ODN might explain the preservation of this response in B Cells from HIV-infected persons despite diminished TLR9 expression. Impaired responsiveness to TLR9 agonists may contriBute to defects in humoral immunity in HIV infection.
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TLR9 stimulation drives naïve B Cells to proliferate and to attain enhanced antigen presenting function.
European journal of immunology, 2007Co-Authors: Wei Jiang, Michael M. Lederman, Clifford V. Harding, Benigno Rodriguez, Richard J. Mohner, Scott F. SiegAbstract:Mechanisms that regulate <B>NaiveB> B Cell proliferation and function are incompletely defined. In this study, we test the hypothesis that <B>NaiveB> B Cell expansion, survival and aBility to present antigen to T lymphocytes can Be directly modulated By Toll-like receptor (TLR) agonists. In the aBsence of B Cell receptor stimulation, CpG oligonucleotide, a TLR9 agonist, was particularly efficient in inducing <B>NaiveB> B Cell proliferation and survival. Although the expanded <B>NaiveB> B Cells did not mature into CD27+ or IgG+ memory B Cells, these Cells did differentiate into IgM-secreting Cells with increased surface expression of HLA-DR, CD40 and CD80. This was associated with an increased potential for these B Cells to activate allogeneic T Cells. We propose that the activation and expansion of <B>NaiveB> B Cells induced By TLR9 agonists could enhance the potential of these Cells to interact with cognate antigens and facilitate Cell-mediated immune responses.
