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  • The American Association of Immunologists  (9)
  • Medicine  (9)
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  • The American Association of Immunologists  (9)
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  • Medicine  (9)
RVK
  • 1
    Online Resource
    Online Resource
    Novel Pattern Recognition Receptor Protects Shrimp by Preventing Bacterial Colonization and Promoting Phagocytosis
    The American Association of Immunologists ; 2017
    In:  The Journal of Immunology Vol. 198, No. 8 ( 2017-04-15), p. 3045-3057
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 198, No. 8 ( 2017-04-15), p. 3045-3057
    Abstract: The recognition of pathogen-associated molecular patterns is accomplished by the recognition modules of pattern recognition receptors (PRRs). Leucine-rich repeats (LRRs) and C-type lectin-like domain (CTLD) represent the two most universal categories of recognition modules. In the current study, we identified a novel soluble and bacteria-inducible PRR comprising LRRs and a CTLD from the hepatopancreas of kuruma shrimp Marsupenaeus japonicus and named it Leulectin. The module arrangement of Leulectin is unique among all organisms. Both modules, together with the whole molecule, protected shrimp against Vibrio infection. By screening the pathogen-associated molecular patterns that shrimp might encounter, Leulectin was found to sense Vibrio flagellin through the LRRs and to recognize LPS through CTLD. The LRR–flagellin interaction was confirmed by pull-down and far-Western assays and was found to rely on the fourth LRR of Leulectin and the N terminus of flagellin. The recognition of LPS was determined by the long loop region of CTLD in a calcium-independent manner. By sensing the flagellin, LRRs could prevent its attachment to shrimp cells, thereby inhibiting Vibrio colonization. With the ability to recognize LPS, CTLD could agglutinate the bacteria and promote hemocytic phagocytosis. Our study clearly showed the division of labor and the synergy between different recognition modules and provided new insights into the concept of pattern recognition and the function of soluble PRRs in the antibacterial response.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1602002
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2017
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    Expression of GM-CSF is regulated by transcription factor Fli-1
    The American Association of Immunologists ; 2019
    In:  The Journal of Immunology Vol. 202, No. 1_Supplement ( 2019-05-01), p. 181.3-181.3
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 202, No. 1_Supplement ( 2019-05-01), p. 181.3-181.3
    Abstract: Granulocyte-macrophage colony-stimulating factor (GM-CSF), also known as colony-stimulating factor 2 (CSF-2) plays an important role in regulating mature myeloid cell populations under both homeostatic and inflammatory conditions. GM-CSF maintains low basal levels under homeostatic conditions, but its levels can quickly become elevated during infection or inflammation. GM-CSF is rapidly produced during inflammatory or autoimmune reactions by a variety of cells, including endothelial cells, macrophages, dendritic cells (DCs), T cells, neutrophils, eosinophils, and more. It has been reported that the expression of GM-CSF is regulated by several transcription factors including NF-kB, AP-1, and RUNX1. Fli-1 belongs to the ETS transcription factor family. We have demonstrated that the Fli-1 transcription factor is a novel regulator in modulating the expression of many inflammatory mediators, including monocyte chemotactic protein 1 (MCP-1), chemokine (C-C motif) ligand 5 (CCL5) and interleukin 6 (IL-6). In this report, we found that murine endothelial cells transfected with Fli-1 specific siRNA produced significant lower levels of GM-CSF after stimulation with Toll-like receptor 4 ligand LPS compared to the cells transfected with control siRNA. Human primary glomerular endothelial cells transfected with Fli-1 specific siRNA had reduced Fli-1 protein and produced significantly less GM-CSF following LPS stimulation compared to the cells transfected with control siRNA. Transient transfection assays show that Fli-1 drives transcription from the GM-CSF promoter in a dose-dependent manner. Together, the results indicate that Fli-1 is a novel, critical transcription factor in regulating the expression of GM-CSF.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.202.Supp.181.3
    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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  • 3
    Online Resource
    Online Resource
    Identification of a Double-β-Defensin with Multiple Antimicrobial Activities in a Marine Invertebrate
    The American Association of Immunologists ; 2023
    In:  The Journal of Immunology Vol. 210, No. 9 ( 2023-05-01), p. 1324-1337
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 210, No. 9 ( 2023-05-01), p. 1324-1337
    Abstract: β-Defensins are a family of cysteine-rich antimicrobial peptides that are generally monodomain. Interestingly, the avian β-defensin 11 (AvBD11) is unique, with two β-defensin motifs with a broad range of antimicrobial activities. However, a double-sized β-defensin has not been identified and functionally characterized in invertebrates. In this study, we cloned and identified a double-β-defensin in shrimp Litopenaeus vannamei (named LvDBD) and explored its potential roles during infection with shrimp pathogens Vibrio parahaemolyticus and white spot syndrome virus (WSSV). LvDBD is an atypical double-sized defensin, which is predicted to possess two motifs related to β-defensin and six disulfide bridges. The RNA interference–mediated knockdown of LvDBD in vivo results in phenotypes with increased bacterial loads, rendering the shrimp more susceptible to V. parahaemolyticus infection, which could be rescued by the injection of recombinant LvDBD protein. In vitro, rLvDBD could destroy bacterial membranes and enhance hemocyte phagocytosis, possibly attributable to its affinity to the bacterial wall components LPS and peptidoglycan. In addition, LvDBD could interact with several viral envelope proteins to inhibit WSSV proliferation. Finally, the NF-κB transcription factors (Dorsal and Relish) participated in the regulation of LvDBD expression. Taken together, these results extend the functional understanding of a double-β-defensin to an invertebrate and suggest that LvDBD may be an alternative agent for the prevention and treatment of diseases caused by V. parahaemolyticus and WSSV in shrimp.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2200817
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2023
    detail.hit.zdb_id: 1475085-5
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  • 4
    Online Resource
    Online Resource
    GITR costimulation redirects regulatory T cells into Th9 cells to promote antitumor immunity (LYM8P.643)
    The American Association of Immunologists ; 2015
    In:  The Journal of Immunology Vol. 194, No. 1_Supplement ( 2015-05-01), p. 201.19-201.19
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 194, No. 1_Supplement ( 2015-05-01), p. 201.19-201.19
    Abstract: GITR is a potent T cell costimulatory molecule with diverse effects on effector and regulatory T cells, and because of this, GITR is of high potential for clinical development including anti-tumor immunity. However, the underlying mechanisms remain unclear. Here, we found that GITR ligation converted iTregs into Th9 cells in vitro. Mechanistically, GITR induced the sustained expression of p50 in activated CD4+ T cells, and p50 then recruited histone deacetylases HDAC1 and Sirt1 to the Foxp3 locus upon binding to the locus; this subsequently led to hypoacetylation, thus resulting in a closed epigenetic configuration of Foxp3 locus. Consistent with this, both p50-/- cells and treatment of HDAC inhibitor rescued iTregs from GITR-mediated suppression. We also found that Foxp3 is a potent repressor of IL-9, mainly through recruiting histone deacetylases to the IL-9 locus, and absence of Foxp3 rendered IL-9 locus accessible. In addition, p50 also promoted the expression of Th9 permissive transcription factors, including PU.1, Batf and Irf4, and all these factors together led to the induction of Th9 cells. Importantly, in a melanoma model in vivo, ligation of GITR using agonistic anti-GITR Ab blocked iTreg differentiation and inhibited tumor progression. In conclusion, our study identifies a new mechanism in which GITR ligation redirects iTregs into Th9 cells to mediate potent anti-tumor immunity. This new finding may have important clinical implications in cancer therapy.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.194.Supp.201.19
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2015
    detail.hit.zdb_id: 1475085-5
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  • 5
    Online Resource
    Online Resource
    Collaboration between a Soluble C-Type Lectin and Calreticulin Facilitates White Spot Syndrome Virus Infection in Shrimp
    The American Association of Immunologists ; 2014
    In:  The Journal of Immunology Vol. 193, No. 5 ( 2014-09-01), p. 2106-2117
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 193, No. 5 ( 2014-09-01), p. 2106-2117
    Abstract: White spot syndrome virus (WSSV) mainly infects crustaceans through the digestive tract. Whether C-type lectins (CLs), which are important receptors for many viruses, participate in WSSV infection in the shrimp stomach remains unknown. In this study, we orally infected kuruma shrimp Marsupenaeus japonicus to model the natural transmission of WSSV and identified a CL (designated as M. japonicus stomach virus–associated CL [MjsvCL]) that was significantly induced by virus infection in the stomach. Knockdown of MjsvCL expression by RNA interference suppressed the virus replication, whereas exogenous MjsvCL enhanced it. Further analysis by GST pull-down and coimmunoprecipitation showed that MjsvCL could bind to viral protein 28, the most abundant and functionally relevant envelope protein of WSSV. Furthermore, cell-surface calreticulin was identified as a receptor of MjsvCL, and the interaction between these proteins was a determinant for the viral infection–promoting activity of MjsvCL. The MjsvCL–calreticulin pathway facilitated virus entry likely in a cholesterol-dependent manner. This study provides insights into a mechanism by which soluble CLs capture and present virions to the cell-surface receptor to facilitate viral infection.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.1400552
    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
    OX40 signaling activates epigenetic mechanisms to repress Th17 cells and Th17-related autoimmune diseases (LYM5P.708)
    The American Association of Immunologists ; 2015
    In:  The Journal of Immunology Vol. 194, No. 1_Supplement ( 2015-05-01), p. 134.13-134.13
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 194, No. 1_Supplement ( 2015-05-01), p. 134.13-134.13
    Abstract: Th17 cells produce copious amount of IL-17, which mediates host antimicrobial responses and autoimmune diseases. The exact mechanisms that control Th17 homeostasis, especially those that inhibit Th17 differentiation, remain incompletely defined. Here, we found that the T cell costimulatory molecule OX40 is a potent repressor of Th17 cells and Th17-mediated autoimmune disease. Under Th17-polarizing conditions in vitro, engagement of OX40 strongly inhibited IL-17 production despite enhanced cell survival and proliferation. Mechanistically, OX40 engagement induced sustained activation of both canonical and non-canonical NF-kB pathways, and it is RelB that mediated dominant suppression of Th17 cells that is independent of p52 and p50. RelB directly recruited H3K9 methyltransferases G9a and Setdb1 upon binding to IL-17 locus, and this resulted in di- and tri-methylation of H3K9, which led to a closed epigenetic configuration of IL-17 locus that prevents RORγt binding to IL-17 locus. Conversely, inhibition of histone methyltransferase activity significantly reversed OX40-mediated suppression of Th17 cells. Importantly, in an EAE model, stimulation of OX40 in vivo inhibited the disease process, while RelB-deficient CD4+ T cells induced exacerbated disease. In conclusion, our study identified a new mechanism in the control of Th17 cells, and this mechanism relies on OX40 induced repressive epigenetic process. This finding may have important therapeutic implications in the clinic.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.194.Supp.134.13
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2015
    detail.hit.zdb_id: 1475085-5
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  • 7
    Online Resource
    Online Resource
    The role of regulatory B cells during the progression of human hepatocellular carcinoma (162.39)
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 1_Supplement ( 2012-05-01), p. 162.39-162.39
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 162.39-162.39
    Abstract: Y SHAO1, CX LI1, YY MA1, XB LIU1, CY CHU2, CC LING1, WH Yeung1, KW Lee3, ST FAN1,2, CM LO1,2, K MAN1,2 1.Department of Surgery 2.Centre for Cancer Research 3. Department of Pathology, The University of Hong Kong, Hong Kong Human regulatory B cells (hBregs) have been shown to play an important role in autoimmune diseases, but their function during human cancer progression remains elusive. In this study, we aim to unveil the underlying mechanism of hBregs regulating human hepatocellular carcinoma (HCC) growth. B cells in HCC liver tumor were examined by immunohistochemistry. We found a tendency that the amount of B cells increased with HCC progression (p=0.001), and it’s in the marginal region of HCC increased (P & lt;0.001) more dramatically. In vitro, human HCC cell line MHCC-97L cells were cocultured with hBregs. hBregs promoted HCC cells proliferation (P=0.011) and migration (p=0.006) and decreased HCC cells apoptosis (p=0.078). HCC cells also promoted hBregs proliferation and migration (p=0.003). hBregs could interact with HCC cells directly through CD40-CD154 signaling. Tail vein injection of hBreg cells into SCID mice increased the size of HCC xenograft tumor (4 weeks, p=0.0221). In vivo imagining showed that hBreg cells could migrate into tumor. Our findings indicate that hBregs could promote HCC progression.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.188.Supp.162.39
    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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  • 8
    Online Resource
    Online Resource
    Expression of GM-CSF Is Regulated by Fli-1 Transcription Factor, a Potential Drug Target
    The American Association of Immunologists ; 2021
    In:  The Journal of Immunology Vol. 206, No. 1 ( 2021-01-01), p. 59-66
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 206, No. 1 ( 2021-01-01), p. 59-66
    Abstract: Friend leukemia virus integration 1 (Fli-1) is an ETS transcription factor and a critical regulator of inflammatory mediators, including MCP-1, CCL5, IL-6, G-CSF, CXCL2, and caspase-1. GM-CSF is a regulator of granulocyte and macrophage lineage differentiation and a key player in the pathogenesis of inflammatory/autoimmune diseases. In this study, we demonstrated that Fli-1 regulates the expression of GM-CSF in both T cells and endothelial cells. The expression of GM-CSF was significantly reduced in T cells and endothelial cells when Fli-1 was reduced. We found that Fli-1 binds directly to the GM-CSF promoter using chromatin immunoprecipitation assay. Transient transfection assays indicated that Fli-1 drives transcription from the GM-CSF promoter in a dose-dependent manner, and mutation of the Fli-1 DNA binding domain resulted in a significant loss of transcriptional activation. Mutation of a known phosphorylation site within the Fli-1 protein led to a significant increase in GM-CSF promoter activation. Thus, direct binding to the promoter and phosphorylation are two important mechanisms behind Fli-1–driven activation of the GM-CSF promoter. In addition, Fli-1 regulates GM-CSF expression in an additive manner with another transcription factor Sp1. Finally, we demonstrated that a low dose of a chemotherapeutic drug, camptothecin, inhibited expression of Fli-1 and reduced GM-CSF production in human T cells. These results demonstrate novel mechanisms for regulating the expression of GM-CSF and suggest that Fli-1 is a critical druggable regulator of inflammation and immunity.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2000664
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2021
    detail.hit.zdb_id: 1475085-5
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  • 9
    Online Resource
    Online Resource
    OX40 ligation recruits the E3 ubiquitin ligases TRAF6 and cIAP2 that cooperatively activate the non-canonical NF-κB pathway (IRM15P.608)
    The American Association of Immunologists ; 2015
    In:  The Journal of Immunology Vol. 194, No. 1_Supplement ( 2015-05-01), p. 199.20-199.20
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 194, No. 1_Supplement ( 2015-05-01), p. 199.20-199.20
    Abstract: The signaling cascades triggered by OX40 in the control of diverse responses from initial T cell activation to the generation of memory and regulatory T cells remain incompletely defined. OX40 preferentially activates and sustains the non-canonical NF-κB pathway, but the underlying mechanisms remain unknown. Here, we found that in primary CD4+ T cells activated under OX40 costimulation, TRAF6 and cIAP2 are two essential molecules and both cooperatively activate the non-canonical NF-κB pathway. Mechanistically, OX40 directly recruited TRAF6 and TRAF2/TRAF3/cIAP2/NIK complexes in which TRAF6 acted as the E3 ligase to mediate Lys63-linked polyubiquitination of cIAP2. Consequently, cIAP2 used its E3 ligase activity to promote TRAF3 Lys48-linked polyubiquitination and degradation. The UBA domain of cIAP2 inhibited the E3 ligase activity of cIAP2 targeting to TRAF3 and this autoinhibition could be released by the C-terminal RING domain polyubiquitination mediated by TRAF6. The lysines 585 and 594 at cIAP2 C-terminus were two main ubiquitin acceptor sites for TRAF6-mediated polyubiquitination, as combined mutation of such sites abolished Lys48-linked TRAF3 polyubiquitination. Thus, in TRAF6 knockout T cells, OX40 failed to induce sufficient non-canonical NF-κB activation and the downstream IL-9 production due to insufficient TRAF3 degradation. Our study identifies a previously unknown mechanism of OX40 controlled non-canonical NF-κB activation in T cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.194.Supp.199.20
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2015
    detail.hit.zdb_id: 1475085-5
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