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  • The American Association of Immunologists  (15)
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  • The American Association of Immunologists  (15)
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  • 1
    Online Resource
    Online Resource
    Immunoglobulin Fc fragment tagging allows strong activation of endogenous CD4 T cells to re-shape the tumor milieu and enhance the antitumor effect of lentivector immunization (162.4)
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 1_Supplement ( 2012-05-01), p. 162.4-162.4
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 162.4-162.4
    Abstract: A major problem with current cancer vaccines is that the induction of CD8 immune responses is rarely associated with antitumor benefits mainly due to the multiple immune suppressions in the established tumor lesions. In this study, we investigated if and how activation of endogenous CD4 T cells could be achieved to relieve the suppressive tumor milieu. We engineered a lentivector to express a nominal fusion Ag composed of HBsAg and IgG2a Fc fragment (HBS-Fc-lv) to increase the magnitude of CD8 response, but more importantly, to induce effective CD4 co-activation. We found that, remarkably, HBS-Fc-lv immunization caused significant regression of established tumors. Immunological analysis revealed that HBS-Fc-lv immunization markedly increased the number of functional CD8 and CD4 T cells and the level of Th1/Tc1-like cytokines in the tumor, while substantially decreased Treg ratio. The favorable immunologic changes in tumor lesions and the improvement of antitumor effects from HBS-Fc-lv immunization were dependent on the Fc receptor mediated CD4 activation. Adoptive transfer of the CD4 T cells from the HBS-Fc-lv immunized mice could activate endogenous CD8 T cells via IFNgamma and CD40L dependent manner. We conclude that endogenous CD4 T cells can be activated by lentivector expressing Fc tagged Ag to provide another layer of help, i.e. creating a pro-inflammatory milieu within the tumor lesion to help the effector phase of immune responses to enhance the antitumor effect.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.188.Supp.162.4
    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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  • 2
    Online Resource
    Online Resource
    miR-338-5p indirectly regulate BAFF signal by targeting TRAF3 during renal allograft antibody-mediated rejection (P2200)
    The American Association of Immunologists ; 2013
    In:  The Journal of Immunology Vol. 190, No. 1_Supplement ( 2013-05-01), p. 69.38-69.38
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 190, No. 1_Supplement ( 2013-05-01), p. 69.38-69.38
    Abstract: Objective: To investigate the regulation mechanism of B cell activating factor (BAFF) signal during antibody-mediated renal allograft rejection (ABMR), microRNAs chip assay and further studies were carried out. Methods: The renal allograft tissues were diagnosed according to Banff'2005 criteria. MicroRNA chip assay was done (tested group: 4 ABMR tissues with high expression of BAFF and C4d; controlled group: 4 IF-TA tissues with no expression of BAFF and C4d). 20 other renal allograft tissues were chosen for differentially expression microRNAs testification, and TRAF3, BAFF and BAFF-R detection by IHC. Dual-lucifirase assay and further functional experiments were taken. Results: microRNA chip assay indicated that miR-200c, miR-30c, let-7b, miR-30b, and 7 other microRNAs were differentially up-regulated and only miR-338-5p was significantly down-regulated. Combing with research background, bioinformatics analysis suggested that TRAF3 was the target gene of miR-338-5p and only regulated by miR-338-5p, which was testified by luciferase assay. The real-time PCR data indicated that miR-338-5p was significantly down-regulated in ABMR tissues, and inversely correlated with BAFF, BAFF-R and TRAF3 (these three molecules high expressed in ABMR tissues). And miR-338-5p mimics and inhibitors can seperately stimulate and inhibit IgG secretion by tonsil B cells in vitro. Conclusions: miR-338-5p participate in ABMR by indirectly regulating BAFF signal via targeting TRAF3.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.190.Supp.69.38
    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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  • 3
    Online Resource
    Online Resource
    Blockade of Programmed Death-1 Pathway Rescues the Effector Function of Tumor-Infiltrating T Cells and Enhances the Antitumor Efficacy of Lentivector Immunization
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 185, No. 9 ( 2010-11-01), p. 5082-5092
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 185, No. 9 ( 2010-11-01), p. 5082-5092
    Abstract: Despite intensive effort, the antitumor efficacy of tumor vaccines remains limited in treating established tumors regardless of the potent systemic tumor-specific immune response and the increases of tumor infiltration of T effector cells. In the current study, we demonstrated that although lentivector (lv) immunization markedly increased Ag-dependent tumor infiltration of CD8 and CD4 T cells and generated Ag-specific antitumor effect, it simultaneously increased the absolute number of myeloid-derived suppressor cells and regulatory T cells in the tumor lesions. In addition, lv immunization induced expression of programmed death-ligand 1 in the tumor lesions. Furthermore, the tumor-infiltrating CD8 T cells expressed high levels of programmed death-1 and were partially dysfunctional, producing lower amounts of effector cytokines and possessing a reduced cytotoxicity. Together, these immune-suppression mechanisms in the tumor microenvironment pose a major obstacle to effective tumor immunotherapy and may explain the limited antitumor efficacy of lv immunization. The loss of effector function in the tumor microenvironment is reversible, and the effector function of CD8 T cells in the tumor could be partially rescued by blocking programmed death-1 and programmed death-ligand 1 pathway in vitro and in vivo, resulting in enhanced antitumor efficacy of lv immunization. These data suggest that immunization alone may exacerbate immune suppression in the tumor lesions and that methods to improve the tumor microenvironment and to rescue the effector functions of tumor-infiltrating T cells should be incorporated into immunization strategies to achieve enhanced antitumor efficacy.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1001821
    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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  • 4
    Online Resource
    Online Resource
    Analysis of Gene Expression and TCR/B Cell Receptor Profiling of Immune Cells in Primary Sjögren’s Syndrome by Single-Cell Sequencing
    The American Association of Immunologists ; 2022
    In:  The Journal of Immunology Vol. 209, No. 2 ( 2022-07-15), p. 238-249
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 209, No. 2 ( 2022-07-15), p. 238-249
    Abstract: Primary Sjögren’s syndrome (pSS) is a chronic autoimmune disease that is estimated to affect 35 million people worldwide and is characterized by lymphocytic infiltration, elevated circulating autoantibodies, and proinflammatory cytokines. The key immune cell subset changes and the TCR/BCR repertoire alterations in pSS patients remain unclear. In this study, we sought to comprehensively characterize the transcriptional changes in PBMCs of pSS patients by single-cell RNA sequencing and single-cell V(D)J sequencing. Naive CD8+ T cells and mucosal-associated invariant T cells were markedly decreased but regulatory T cells were increased in pSS patients. There were a large number of differentially expressed genes shared by multiple subpopulations of T cells and B cells. Abnormal signaling pathways, including Ag processing and presentation, the BCR signaling pathway, the TCR signaling pathway, and Epstein–Barr virus infection, were highly enriched in pSS patients. Moreover, there were obvious differences in the CD30, FLT3, IFN-II, IL-1, IL-2, IL-6, IL-10, RESISTIN, TGF-β, TNF, and VEGF signaling networks between pSS patients and healthy controls. Single-cell TCR and BCR repertoire analysis showed that there was a lower diversity of T cells in pSS patients than in healthy controls; however, there was no significant difference in the degree of clonal expansion, CDR3 length distribution, or degree of sequence sharing. Notably, our results further emphasize the functional importance of αβ pairing in determining Ag specificity. In conclusion, our analysis provides a comprehensive single-cell map of gene expression and TCR/BCR profiles in pSS patients for a better understanding of the pathogenesis, diagnosis, and treatment of pSS.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2100803
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2022
    detail.hit.zdb_id: 1475085-5
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  • 5
    Online Resource
    Online Resource
    IL-15 enhances the anti-tumor effect of human tumor antigen-specific T cells by cellular senescence delay (TUM2P.880)
    The American Association of Immunologists ; 2014
    In:  The Journal of Immunology Vol. 192, No. 1_Supplement ( 2014-05-01), p. 71.4-71.4
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 192, No. 1_Supplement ( 2014-05-01), p. 71.4-71.4
    Abstract: Optimal expansion protocol for adoptive T-cell therapy often include interleukin (IL)-15, however, the mechanism by which IL-15 improves the in vivo anti-tumor effect of T cells remains to be elucidated. Using T cells generated from HLA-A2+ normal donors against novel T-cell epitopes derived from the U266 myeloma Ig light chain V-region (idiotype) as a model, we confirmed that T cells cultured with IL-15 provide more potent anti-tumor effects than IL-2-cultured T cells, after adoptive transfer in vivo into immunodeficient hosts. This effect was associated with delayed/reversed senescence in IL-15 expanded idiotype-specific memory CD8 T cells. In vitro experiments revealed IL-15 mediated senescence delay/reversal through JAK3-STAT5 and IL-2 receptor βγ signaling pathway. Specifically, we found DNA damage molecules MDC1, 53BP1, and ATM are the direct targets of IL-15 signaling and STAT5 represses the promoter activity of these genes through the competition with STAT3 to bind to the STATs sites. Thus, our study provides the first evidence for IL-15-inducing the repression of transcription of DNA damage molecules and senescence delay in human memory CD8 T cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.192.Supp.71.4
    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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  • 6
    Online Resource
    Online Resource
    Promotion of engraftment by donor NK cell infusion and IL-15 in nonmyeloablative allogeneic bone marrow transplantation (145.18)
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 1_Supplement ( 2010-04-01), p. 145.18-145.18
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 145.18-145.18
    Abstract: Donor NK cells have been shown to be able to promote engraftment during allogeneic bone marrow transplantation (allo-BMT). The biological activity of NK cells can be significantly enhanced by IL-15. We carried out experiments to determine the effects of combining donor NK cell infusion and IL-15 administration in a murine nonmyeloablative allo-BMT model. Mice infused with donor NK cells and treated with IL-15 during BMT resulted in increased donor engraftment compared with either treatment alone, although single treatment could also significantly promote donor engraftment. The counts of donor derived cell subsets were all increased in the spleens of the recipient mice with combinational treatment compared with either treatment alone. The alloreactivity to donor type antigens was significantly reduced in the recipient mice with combinational treatment, which was manifested by decreased proliferation and IL-2 secretion of splenocytes from recipient mice in response to donor type antigens in mixed lymphocyte responses and decreased capacity of the splenocytes killing donor type tumor targets. In conclusion, the combination of donor NK cell infusion and IL-15 administration could promote donor engraftment and development of all donor derived cell subsets, as well as suppress the host allo-responses in a nonmyeloablative allo-BMT model. The results provide a promising way to promote donor engraftment without involving systemic and nonspecific suppression of the immune system.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.184.Supp.145.18
    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
    Activation of endogenous CD4 T cells stimulates favorable immunologic changes in the tumor milieu and enhances the antitumor effect of lentivector immunization (48.15)
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 1_Supplement ( 2011-04-01), p. 48.15-48.15
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 1_Supplement ( 2011-04-01), p. 48.15-48.15
    Abstract: CD4 T cells are known to help the induction, migration, and effector functions of CD8 antitumor responses. Here, we reported an additional layer of CD4 helper function, i.e. activation of endogenous CD4 T cells could modulate the tumor milieu. We engineered a lentivector to express a nominal fusion Ag composed of hepatitis B surface protein (HBsAg) and IgG2a Fc domain (HBS-Fc-lv) that induced potent CD8 as well as robust CD4 response. Remarkably, immunization with this vector caused regression of established tumors. Immunological analysis revealed that functional CD8 and CD4 T effector (Teff) was markedly increased while the Treg ratio was substantially decreased in the regressing tumors. HBS-Fc-lv immunization also shifted the suppressive tumor lesion microenvironment to one that is immune stimulating. Mechanistically, the decrease of tumor Treg ratio and the improvement of antitumor effect of HBS-Fc-lv immunization were dependent on CD4 activation and IFNg production. CD4 Teff cells were preferentially expanded in the vaccine draining lymph nodes and selectively recruited into tumor lesions as the chemokines for Teff recruitment were significantly increased in the tumor lesions after HBS-Fc-lv immunization. These data indicate that immunization strategies capable of activating both CD8 and CD4 T cells can improve the tumor milieu and generate an enhanced antitumor effect.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.186.Supp.48.15
    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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  • 8
    Online Resource
    Online Resource
    Crosstalk of BAFF and TLRs after HCMV Infection in renal transplantation recipients (TRAN3P.878)
    The American Association of Immunologists ; 2014
    In:  The Journal of Immunology Vol. 192, No. 1_Supplement ( 2014-05-01), p. 202.17-202.17
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 192, No. 1_Supplement ( 2014-05-01), p. 202.17-202.17
    Abstract: To investigate the correlation of BAFF signal and TLRs activtion after HCMV infection in renal transplant (RTx) recipients. Peripheral blood and urine of RTx recipients (113 cases) were collected. Urine HCMV DNA was detected by quantitative real-time PCR (qPCR); Sera anti-pp65 IgG /IgM antibody were detected with the use of HCMV pp65 antigen slide by indirect immunofluorescence assay; Soluble BAFF (sBAFF) was tested by ELISA; Sera anti-HLA & MICA was determined by single-antigen flow bead assays (One Lambda) on a Luminex platform; The concerned genes selected by Gene Ontology (GO) function classification and KEGG Pathway analysis were tested by qPCR chip assay. In RTx recipients with high copy of urine HCMV DNA ( & gt;10,000 copy/ml, 12 cases, positive group), sBAFF, anti-pp65 antibody, and anti-HLA & MICA antibody also increased (P & lt;0.05); The correlation analysis indicated that HCMV DNA level was positively related with sBAFF, anti-pp65 antibody, and anti-HLA & MICA antibody. And the qPCR chip assay results showed that 46 genes were differentially expressed ( & gt; 2 times) in all. In positive group BAFF-R and ICAM1 were upregulated, TLR9, NLRC5 and other 20 genes were downregulated, compared with negative group (with low copy of HCMV DNA); IFN-γ and ICAM1 were upregulated and 8 genes were downregulated in positive group, compared with healthy controls. So BAFF signal was enhanced after HCMV infection in RTx recipients, which involved in the decrease of renal allograft function.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.192.Supp.202.17
    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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  • 9
    Online Resource
    Online Resource
    m6A RNA modification controls transitions between quiescence and proliferation during B cell development
    The American Association of Immunologists ; 2019
    In:  The Journal of Immunology Vol. 202, No. 1_Supplement ( 2019-05-01), p. 53.19-53.19
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 202, No. 1_Supplement ( 2019-05-01), p. 53.19-53.19
    Abstract: N6-methyladenosine (m6A) is the most abundant internal modification in eukaryotic mRNA. Recent conceptual and technological advances have sparked extensive research interests in the functional roles of m6A. The writers, erasers and readers of m6A have been identified and characterized in a number of biological processes in recent years. However, the physiological roles of m6A and its effectors in lymphogenesis remained unknown. Here, we report that loss of METTL14, a core component of the m6A writer complex, in mouse B lineage cells blocked B cell development. Deletion of METTL14 in developing B cells caused dramatic reductions in the mRNA m6A level, together with an incomplete blockage during the transition from the quiescent pro-B stage to the proliferating large pre-B stage as well as a complete blockage during the proliferation-to-quiescence transition between large pre-B and small pre-B stages. We found that & gt;67% transcripts contain m6A in developing B cells, suggesting that m6A might be widely involved in gene expression regulation. m6A controlled the quiescence-to-proliferation switch partially through its cytoplasmic reader YTHDF2, as deleting YTHDF2 partially mimicked the earlier incomplete blockage between pro-B and large pre-B stages due to METTL14 deficiency, but did not cause the later proliferation-to-quiescence blockage. Altogether, our data identifies m6A, which specifically controls transitions between quiescence and proliferation, as a critical new layer of gene expression regulation in B cell development.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.202.Supp.53.19
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2019
    detail.hit.zdb_id: 1475085-5
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  • 10
    Online Resource
    Online Resource
    Sera miR-338-5p differentially expressed in renal transplant recipients and negatively related with soluble BAFF (TRAN3P.877)
    The American Association of Immunologists ; 2014
    In:  The Journal of Immunology Vol. 192, No. 1_Supplement ( 2014-05-01), p. 202.16-202.16
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 192, No. 1_Supplement ( 2014-05-01), p. 202.16-202.16
    Abstract: To investigate the expression characteristic of sera miR-338-5p in renal transplant (RTx) recipients, and further analyse its potential significance. Serum of RTx recipients (49 cases) were collected. miR-338-5p were extracted and detected by qPCR, soluble B cell activating factor (sBAFF) was determined by ELISA (R & D), and the presence of circulating anti-HLA & MICA was determined by single-antigen flow bead assays (One Lambda) on a Luminex platform. Healthy volunteers (20 cases) were controls. SPSS17.0 software was applied, two-side t-test was to analyse the means of two-independent samples, Spearman method was to analyse the correlation of miR-338-5p and sBAFF, anti-HLA & MICA. P & lt;0.05 was considered to be significant. Compared with healthy controls, miR-338-5p in RTx recipients significantly decreased and sBAFF significantly increased (P & lt;0.05). miR-338-5p significantly down-regulated in RTx recipients within 1-year post-operation, compared with those over 1-year post-operation (P & lt;0.05); miR-338-5p also signficantly down-regulated in recipients within 3-year post-operation, comapred with those over 3-year post-operation (P & lt;0.05). sBAFF level in different period after operation was not significant. For all subjects, miR-338-5p was negatively correlated with sBAFF (r=-0.51, P & lt;0.001), and sBAFF was positively correlated with anti-MICA antibody (r=0.86, P & lt;0.05). miR-338-5p may involve in the procedure of immune response after RTx by indirectly or directly targeting BAFF signal.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.192.Supp.202.16
    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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