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  • The American Association of Immunologists  (4)
  • Feng, Jianxun  (4)
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  • The American Association of Immunologists  (4)
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  • 1
    Online Resource
    Online Resource
    IFN Regulatory Factor 8 Restricts the Size of the Marginal Zone and Follicular B Cell Pools
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 3 ( 2011-02-01), p. 1458-1466
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 3 ( 2011-02-01), p. 1458-1466
    Abstract: Transcriptional control of marginal zone (MZ) and follicular (FO) B cell development remains incompletely understood. The transcription factor, IFN regulatory factor (IRF)8, is known to play important roles in the differentiation of early B cells. In this article, we demonstrate that IRF8 is also required for normal development of MZ and FO B cells. Mice with a conventional knockout of Irf8 (IRF8−/−) or a point mutation in the IRF association domain of IRF8 had increased numbers of MZ B cells. To determine the B cell-intrinsic effects of IRF8 deficiency, we generated mice with a conditional allele of Irf8 crossed with CD19-Cre mice (designated IRF8-conditional knockout [CKO]). These mice had enlarged MZ and increased numbers of MZ and FO B cells compared with controls. The FO B cells of CKO mice exhibited reduced expression of CD23 and moderately increased expression of CD21. Gene-expression profiling showed that increased B cell production in IRF8-CKO mice was associated with changes in expression of genes involved in regulation of transcription, signaling, and inflammation. Functional studies showed that IRF8-CKO mice generated normal Ab responses to T-independent and T-dependent Ags. Thus, IRF8 controls the expansion and maturation of MZ and FO B cells but has little effect on B cell function.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1001950
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Transitional B Cells Lose Their Ability to Receptor Edit but Retain Their Potential for Positive and Negative Selection
    The American Association of Immunologists ; 2007
    In:  The Journal of Immunology Vol. 179, No. 11 ( 2007-12-01), p. 7544-7552
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 179, No. 11 ( 2007-12-01), p. 7544-7552
    Abstract: Ligation of B cell receptors on immature bone marrow B cells, either by an endogenous Ag or by an anti-B cell receptor Ab induces secondary V(D)J gene rearrangements, termed receptor editing. Whether the same signal induces receptor editing in transitional B cells is not clear. In this study, we examined the responses of immature and transitional B cells from VH12Vκ1A Ig transgenic mice to stimulation with an anti-Igβ Ab. Our results demonstrated that immature B cells stimulated with a low concentration of anti-Igβ Ab, mimicking Ag stimulation, underwent receptor editing both in vivo and in vitro, as evidenced by the detection of dsDNA breaks at Jκ recombination signal sequences, whereas transitional B cells did not. The lack of dsDNA breaks in transitional B cells contrasts with their increased expression of RAG1 and RAG2, suggesting a novel mechanism that may prevent rearrangements. Furthermore, treatment of transitional B cells with high concentrations of anti-Igβ Abs induced apoptosis, whereas low concentrations induced differentiation. Our results support the idea that transitional B cells lose the capacity to edit, but are sensitive to positive and negative selection.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.179.11.7544
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2007
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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    Online Resource
  • 3
    Online Resource
    Online Resource
    ENPP1 is a novel cell surface marker of germinal center and memory B cells and is highly expressed in plasma cells (36.3)
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 1_Supplement ( 2010-04-01), p. 36.3-36.3
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 36.3-36.3
    Abstract: The ectonucleotide pyrophosphatase phosphodiesterase 1 (ENPP1), also known as plasma cell (PC) alloantigen 1 (PC-1), is expressed on PCs and many non-lymphoid tissues. ENPP1 hydrolyzes NTP to generate NMP and pyrophosphate (PPi). PPi is an important factor for controlling mineralization of the bone. In addition, ENPP1 directly associates with the insulin receptor and regulates insulin receptor signaling. Abnormal expression of ENPP1 has been associated with diabetes and insulin resistance. Although ENPP1 was first identified in PCs, its expression and function in B lineage cells remains poorly understood. Here we describe a previously unknown expression pattern of ENPP1 in murine late stage B cells. By using an anti-ENPP1 mAb and flow cytometry, we found that the expression levels of ENPP1 in early and mature naïve B cells were relatively low. However, germinal center (GC) B cells, PCs and memory B cells expressed 2-4-fold more ENPP1 than resting B cells. Moreover, gene expression profiling studies of primary lymphomas in NFS.V+ congenic mice revealed high expression levels of ENPP1 in plasmacytomas, immunoblastic lymphomas, and centroblastic-follicular lymphoma types, corresponding with their PC and GC origins. These studies demonstrate that ENPP1 can be a useful marker for identification of stages in GC and post-GC cell differentiation and of lymphomas with a GC or PC origin. The function of ENPP1 in B cells is currently under investigation.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.184.Supp.36.3
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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    Online Resource
  • 4
    Online Resource
    Online Resource
    Functional deficiency in IL-7 caused by an ENU-induced point mutation (82.11)
    The American Association of Immunologists ; 2007
    In:  The Journal of Immunology Vol. 178, No. 1_Supplement ( 2007-04-01), p. S111-S111
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 178, No. 1_Supplement ( 2007-04-01), p. S111-S111
    Abstract: N-ethyl-N-nitrosourea (ENU)-induced mutagenesis provides a powerful approach to identifying genes involved in immune regulation and diseases. Here we describe a new mutant strain, HLB368, with hereditary leukopenia. At necropsy, the mutant mice had very small thymuses and spleens. All but the inguinal nodes were absent and there were no Peyer’s patches. By flow cytometry, the ratios of T cell subsets were normal, but B cell development was blocked at the pre-pro-B cell stage. The development of B1 and marginal zone B cells was relatively normal. The mutation was mapped to chromosome 3 between D3Mit221 and D3Mit224, a region that contains the Il7 gene. cDNA and genomic DNA sequences of Il7 revealed a T-to-C missense transition resulting in a change of Leu to Pro within the leader peptide that would be predicted to inhibit secretion. In keeping with this concept, we found that in vitro treatment of B cell progenitors from mutant mice with IL-7 induced them to differentiate into pre-BII cells. Phenotypic comparisons of HLB368 with genetically targeted Il7 null mice showed many similarities along with a few differences, indicating that this ENU-induced mutant carries a novel allele. This new strain thus provides a new model for studying the functions of IL-7 on a pure C57BL/6 background.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.178.Supp.82.11
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2007
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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    Online Resource
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