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  • 1
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    Online Resource
    The fission yeast pleckstrin homology domain protein Spo7 is essential for initiation of forespore membrane assembly and spore morphogenesis
    American Society for Cell Biology (ASCB) ; 2011
    In:  Molecular Biology of the Cell Vol. 22, No. 18 ( 2011-09-15), p. 3442-3455
    Details
    In: Molecular Biology of the Cell, American Society for Cell Biology (ASCB), Vol. 22, No. 18 ( 2011-09-15), p. 3442-3455
    Abstract: Sporulation in fission yeast represents a unique mode of cell division in which a new cell is formed within the cytoplasm of a mother cell. This event is accompanied by formation of the forespore membrane (FSM), which becomes the plasma membrane of spores. At prophase II, the spindle pole body (SPB) forms an outer plaque, from which formation of the FSM is initiated. Several components of the SPB play an indispensable role in SPB modification, and therefore in sporulation. In this paper, we report the identification of a novel SPB component, Spo7, which has a pleckstrin homology (PH) domain. We found that Spo7 was essential for initiation of FSM assembly, but not for SPB modification. Spo7 directly bound to Meu14, a component of the leading edge of the FSM, and was essential for proper localization of Meu14. The PH domain of Spo7 had affinity for phosphatidylinositol 3-phosphate (PI3P). spo7 mutants lacking the PH domain showed aberrant spore morphology, similar to that of meu14 and phosphatidylinositol 3-kinase (pik3) mutants. Our study suggests that Spo7 coordinates formation of the leading edge and initiation of FSM assembly, thereby accomplishing accurate formation of the FSM.
    Type of Medium: Online Resource
    ISSN: 1059-1524 , 1939-4586
    URL: Article
    DOI: 10.1091/mbc.e11-02-0125
    Language: English
    Publisher: American Society for Cell Biology (ASCB)
    Publication Date: 2011
    detail.hit.zdb_id: 1474922-1
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Generation of memory B cells inside and outside germinal centers
    Wiley ; 2014
    In:  European Journal of Immunology Vol. 44, No. 5 ( 2014-05), p. 1258-1264
    Details
    In: European Journal of Immunology, Wiley, Vol. 44, No. 5 ( 2014-05), p. 1258-1264
    Abstract: Germinal centers (GCs) are generally considered to be the sole site of memory B‐cell generation. However, recent studies demonstrate that memory B cells can also develop in response to a T‐cell dependent (TD) antigen before the onset, and independently of, the GC reaction. These two classes of memory cells persist equally over long periods of time and attain functional maturation through distinct but related transcriptional programs. Although the development of both memory B‐cell types requires classical T‐cell help, the generation of GC‐dependent memory B cells requires T FH ‐cell help, while the generation of GC‐independent memory cells does not. These findings led to the conclusion that B‐cell memory is generated along two fundamentally distinct cellular differentiation pathways. In this review, we focus on the GC‐independent pathway of memory B‐cell development, and discuss how the unique features of memory B cells are maintained in the GC‐independent pathway.
    Type of Medium: Online Resource
    ISSN: 0014-2980 , 1521-4141
    URL: Issue
    URL: Article
    DOI: 10.1002/eji.v44.5
    DOI: 10.1002/eji.201343716
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 1491907-2
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  • 3
    Online Resource
    Online Resource
    B-lymphoid cells with attributes of dendritic cells regulate T cells via indoleamine 2,3-dioxygenase
    Proceedings of the National Academy of Sciences ; 2010
    In:  Proceedings of the National Academy of Sciences Vol. 107, No. 23 ( 2010-06-08), p. 10644-10648
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 107, No. 23 ( 2010-06-08), p. 10644-10648
    Abstract: A discrete population of splenocytes with attributes of dendritic cells (DCs) and coexpressing the B-cell marker CD19 is uniquely competent to express the T-cell regulatory enzyme indoleamine 2,3-dioxygenase (IDO) in mice treated with TLR9 ligands (CpGs). Here we show that IDO-competent cells express the B-lineage commitment factor Pax5 and surface immunoglobulins. CD19 ablation abrogated IDO-dependent T-cell suppression by DCs, even though cells with phenotypic attributes matching IDO-competent cells developed normally and expressed IDO in response to interferon γ. Consequently, DCs and regulatory T cells (Tregs) did not acquire T-cell regulatory functions after TLR9 ligation, providing an alternative perspective on the known T-cell regulatory defects of CD19-deficient mice. DCs from B-cell–deficient mice expressed IDO and mediated T-cell suppression after TLR9 ligation, indicating that B-cell attributes were not essential for B-lymphoid IDO-competent cells to regulate T cells. Thus, IDO-competent cells constitute a distinctive B-lymphoid cell type with quintessential T-cell regulatory attributes and phenotypic features of both B cells and DCs.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.0914347107
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2010
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Both mutated and unmutated memory B cells accumulate mutations in the course of the secondary response and develop a new antibody repertoire optimally adapted to the secondary stimulus
    Oxford University Press (OUP) ; 2013
    In:  International Immunology Vol. 25, No. 12 ( 2013-12-01), p. 683-695
    Details
    In: International Immunology, Oxford University Press (OUP), Vol. 25, No. 12 ( 2013-12-01), p. 683-695
    Abstract: High-affinity memory B cells are preferentially selected during secondary responses and rapidly differentiate into antibody-producing cells. However, it remains unknown whether only high-affinity, mutated memory B cells simply expand to dominate the secondary response or if in fact memory B cells with a diverse VH repertoire, including those with no mutations, accumulate somatic mutations to create a new repertoire through the process of affinity maturation. In this report, we took a new approach to address this question by analyzing the VH gene repertoire of IgG1+ memory B cells before and after antigen re-exposure in a host unable to generate IgG+ B cells. We show here that both mutated and unmutated IgG1+ memory B cells respond to secondary challenge and expand while accumulating somatic mutations in their VH genes in a stepwise manner. Both types of memory cells subsequently established a VH gene repertoire dominated by two major clonotypes, which are distinct from the original repertoire before antigen re-exposure. In addition, heavily mutated memory B cells were excluded from the secondary repertoire. Thus, both mutated and unmutated IgG1+ memory cells equally contribute to establish a new antibody repertoire through a dynamic process of mutation and selection, becoming optimally adapted to the recall challenge.
    Type of Medium: Online Resource
    ISSN: 1460-2377 , 0953-8178
    URL: Article
    DOI: 10.1093/intimm/dxt030
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2013
    detail.hit.zdb_id: 1467474-9
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  • 5
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    Online Resource
    Analysis of DNA Methylation in Bowel Lavage Fluid for Detection of Colorectal Cancer
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Prevention Research Vol. 7, No. 10 ( 2014-10-01), p. 1002-1010
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 7, No. 10 ( 2014-10-01), p. 1002-1010
    Abstract: Aberrant DNA methylation could potentially serve as a biomarker for colorectal neoplasms. In this study, we assessed the feasibility of using DNA methylation detected in bowel lavage fluid (BLF) for colorectal cancer screening. A total of 508 BLF specimens were collected from patients with colorectal cancer (n = 56), advanced adenoma (n = 53), minor polyp (n = 209), and healthy individuals (n = 190) undergoing colonoscopy. Methylation of 15 genes (miR-1-1, miR-9-1, miR-9-3, miR-34b/c, miR-124-1, miR-124-2, miR-124-3, miR-137, SFRP1, SFRP2, APC, DKK2, WIF1, LOC386758, and ZNF582) was then analyzed in MethyLight assays, after which receiver operating characteristic (ROC) curves were analyzed to assess the diagnostic performance of BLF methylation. Through analyzing BLF specimens in a training set (n = 345), we selected the three genes showing the greatest sensitivity for colorectal cancer detection (miR-124-3, 71.8%; LOC386758, 79.5%; and SFRP1, 74.4%). A scoring system based on the methylation of those three genes (M-score) achieved 82% sensitivity and 79% specificity, and the area under the ROC curve (AUC) was 0.834. The strong performance of this system was then validated in an independent test set (n = 153; AUC = 0.808). No significant correlation was found between M-score and the clinicopathologic features of the colorectal cancers. Our results demonstrate that DNA methylation in BLF specimens may be a useful biomarker for the detection of colorectal cancer. Cancer Prev Res; 7(10); 1002–10. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.CAPR-14-0162
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2422346-3
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  • 6
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    Online Resource
    Correction: Constitutive CD40L Expression on B Cells Prematurely Terminates Germinal Center Response and Leads to Augmented Plasma Cell Production in T Cell Areas
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 185, No. 4 ( 2010-08-15), p. 2631-2631
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 185, No. 4 ( 2010-08-15), p. 2631-2631
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1090070
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
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  • 7
    Online Resource
    Online Resource
    Indoleamine 2,3-dioxygenase inhibits B cell immune response to T independent antigens (IRM8P.710)
    The American Association of Immunologists ; 2014
    In:  The Journal of Immunology Vol. 192, No. 1_Supplement ( 2014-05-01), p. 127.11-127.11
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 192, No. 1_Supplement ( 2014-05-01), p. 127.11-127.11
    Abstract: T cell independent (TI) antibody responses are crucial for humoral immunity to viruses and encapsulated bacteria. Here we report a novel mechanism where the tryptophan catabolizing enzyme indoleamine 2,3-dioxygenase (IDO) 1 regulates the B cell response to TI antigens. Immunization with NP-Ficoll led to rapid splenic induction of IDO, primarily in the extra-follicular space. When IDO1KO mice were immunized there was a significant increase in humoral responses with increased formation of extra-follicular IgM and IgG3 foci, antibody secreting cells (ASCs), and increased antibody titers. This was not associated with an alteration in affinity maturation suggesting the primary impact of IDO1 deficiency was increased B cell proliferation and plasma cell formation. IDO1 did not affect immune responses to protein antigens as immunization with NP-OVA elicited similar antibody titers regardless of IDO1 function. In addition, adoptive transfer of IDO1 deficient B cells to µMT-/- (B cell deficient) mice was sufficient to replicate increased TI responses observed in IDOKO mice. Moreover, in vitro LPS rapidly induced IDO1 in MACS-purified B cells and IDO deficient B cells display enhanced LPS and CpG-driven proliferation associated with increased production of IgM, IgG3, and IL10. Thus, our results demonstrate a novel role of IDO in suppressing T cell independent antibody response that provides insight into the understanding of B cell immune responses in autoimmunity and vaccine biology.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.192.Supp.127.11
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2014
    detail.hit.zdb_id: 1475085-5
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  • 8
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    Online Resource
    Excess B cell CD40/CD40L signaling promotes CD4 T cell-mediated encephalomyelitis in mice (44.22)
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 1_Supplement ( 2011-04-01), p. 44.22-44.22
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 1_Supplement ( 2011-04-01), p. 44.22-44.22
    Abstract: To test the pathogenic role of B cells under excess inflammatory CD40/CD40L signaling, experimental autoimmune encephalomyelitis (EAE) was induced in B cell specific CD40L transgenic (CD40LBTg) and C57BL/6 control mice by immunization with MOG35-55 peptide. Clinical symptoms were monitored using a 0-5 scoring system during days 10-30 after induction. Alternatively, MOG-specific CD4 TCR Tg (2D2) mice were crossed onto a CD40LBTg background and the incidence of spontaneous encephalomyelitis monitored at 4-35 weeks of age. Both CD40LBTg and control mice developed EAE with similar kinetics, with disease onset at around day 15-17 and the peak of disease score at around day 21-25. However, CD40LBTg mice showed significantly more severe disease than wild type mice with average peak clinical scores of 3.0 and 1.5, respectively. Higher frequencies of IL-17+ CD4 T cells were also observed in CD40LBTg mice compared to wild type mice at the EAE disease peak. Also, 60% (6/10) of 2D2 CD40LB double Tg mice showed spontaneous encephalomyelitis-like symptoms (severe hind and/or fore limb paralysis) between 4-6 weeks of age, with IL-17+ and IFNγ+ CD4 T cells in spleen and inguinal lymph nodes. Furthermore, even those without apparent EAE symptoms died before 30 weeks of age. None of the 2D2 or CD40LBTg mice showed such symptoms between 4-35 weeks of age. These results support the notion that excess B cell CD40/CD40L signaling promotes MOG-specific pathogenic CD4 T cell response.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.186.Supp.44.22
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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  • 9
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    Online Resource
    A critical role of dendritic cells in CD8 T cell IL-10 expression during inflammatory response triggered by CD40-activated B cells (159.16)
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 1_Supplement ( 2012-05-01), p. 159.16-159.16
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 159.16-159.16
    Abstract: CD40LBTg mice, expressing a CD40 ligand (CD40L) transgene on B cells, represent a model for human diseases where B cells aberrantly express CD40L or receive excess CD40/CD40L signaling under inflammatory conditions. Here, we show that B cells expressing transgenic CD40L are capable of priming CD8 T cells and generate strong antigen-specific cytotoxicity. Adoptively transferred SIINFEKL peptide-loaded B cells from CD40LBTg but not wild type mice were able to activate self-reactive OT-I CD8 T cells upon immunization with OVA plus alum and trigger diabetes in RIP-OVA mice by enhancing the help of endogenous self-reactive CD4 T cells. CD40L expressing B cells also trigger spontaneous activation of splenic CD8 T cells, which rapidly up-regulate PD-1, Blimp-1 and LAG-3 and lose cytotoxicity along with IL-10 expression via interaction with PDL-1hi CD11c+ dendritic cells in T cell zones. Thus, CD11c+ dendritic cells from CD40LBTg mice exhibit regulatory phenotype, which block granzyme B expression and preferentially induce IL-10 expression in activated CD8 T cells. These results demonstrate that constitutive CD40 signaling on B cells under inflammation increases the risk of breaking peripheral CD8 T cell tolerance. However, the presence of CD40-activated B cells results in PDL-1hi CD11c+ dendritic cells, which exhibit a regulatory role to dampen harmful self-reactive cytotoxicity by promoting IL-10 expression in CD8 T cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.188.Supp.159.16
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2012
    detail.hit.zdb_id: 1475085-5
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  • 10
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    Online Resource
    Constitutively CD40–Activated B Cells Regulate CD8 T Cell Inflammatory Response by IL-10 Induction
    The American Association of Immunologists ; 2013
    In:  The Journal of Immunology Vol. 190, No. 7 ( 2013-04-01), p. 3189-3196
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 190, No. 7 ( 2013-04-01), p. 3189-3196
    Abstract: B cells are exposed to high levels of CD40 ligand (CD40L, CD154) in chronic inflammatory diseases. In addition, B cells expressing both CD40 and CD40L have been identified in human diseases such as autoimmune diseases and lymphoma. However, how such constitutively CD40–activated B cells under inflammation may impact on T cell response remains unknown. Using a mouse model in which B cells express a CD40L transgene (CD40LTg) and receive autocrine CD40/CD40L signaling, we show that CD40LTg B cells stimulated memory-like CD4 and CD8 T cells to express IL-10. This IL-10 expression by CD8 T cells was dependent on IFN-I and programmed cell death protein 1, and was critical for CD8 T cells to counterregulate their overactivation. Furthermore, adoptive transfer of naive CD8 T cells in RAG-1−/− mice normally induces colitis in association with IL-17 and IFN-γ cytokine production. Using this model, we show that adoptive cotransfer of CD40LTg B cells, but not wild-type B cells, significantly reduced IL-17 response and regulated colitis in association with IL-10 induction in CD8 T cells. Thus, B cells expressing CD40L can be a therapeutic goal to regulate inflammatory CD8 T cell response by IL-10 induction.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1203364
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2013
    detail.hit.zdb_id: 1475085-5
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