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  • Jin, Xiaoqian  (3)
  • 1
    Online Resource
    Online Resource
    S100A4 Is Critical for a Mouse Model of Allergic Asthma by Impacting Mast Cell Activation
    Frontiers Media SA ; 2021
    In:  Frontiers in Immunology Vol. 12 ( 2021-7-22)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 12 ( 2021-7-22)
    Abstract: The calcium-binding protein S100A4 demonstrates important regulatory roles in many biological processes including tumorigenesis and inflammatory disorders such as allergy. However, the specific mechanism of the contribution of S100A4 to allergic diseases awaits further clarification. Objective To address the effect of S100A4 on the regulation of mast cell activation and its impact on allergy. Methods Bone marrow-derived cultured mast cells (BMMCs) were derived from wild-type (WT) or S100A4 -/- mice for in vitro investigation. WT and S100A4 -/- mice were induced to develop a passive cutaneous anaphylaxis (PCA) model, a passive systemic anaphylaxis (PSA) model, and an ovalbumin (OVA)-mediated mouse asthma model. Results Following OVA/alum-based sensitization and provocation, S100A4 -/- mice demonstrated overall suppressed levels of serum anti-OVA IgE and IgG antibodies and proinflammatory cytokines in serum, bronchoalveolar lavage fluid (BALF), and lung exudates. S100A4 -/- mice exhibited less severe asthma signs which included inflammatory cell infiltration in the lung tissue and BALF, and suppressed mast cell recruitment in the lungs. Reduced levels of antigen reencounter-induced splenocyte proliferation in vitro were recorded in splenocytes from OVA-sensitized and challenged mice that lacked S100A4 -/- . Furthermore, deficiency in the S100A4 gene could dampen mast cell activation both in vitro and in vivo , evidenced by reduced β-hexosaminidase release and compromised PCA and PSA reaction. We also provided evidence supporting the expression of S100A4 by mast cells. Conclusion S100A4 is required for mast cell functional activation, and S100A4 may participate in the regulation of allergic responses at least partly through regulating the activation of mast cells.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2021.692733
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2606827-8
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  • 2
    Online Resource
    Online Resource
    Dysregulated T Cell Activation and Aberrant Cytokine Expression Profile in Systemic Lupus Erythematosus
    Hindawi Limited ; 2019
    In:  Mediators of Inflammation Vol. 2019 ( 2019-03-17), p. 1-11
    Details
    In: Mediators of Inflammation, Hindawi Limited, Vol. 2019 ( 2019-03-17), p. 1-11
    Abstract: Accumulating evidence indicates a critical role for T cells and relevant cytokines in the pathogenesis of systemic lupus erythematosus (SLE). However, the specific contribution of T cells together with the related circulating cytokines in disease pathogenesis and organ involvement is still not clear. In the current study, we investigated relevant molecule expressions and cytokine levels in blood samples from 49 SLE patients and 22 healthy control subjects. The expression of HLA-DR and costimulatory molecules on T cells was evaluated by flow cytometry. Concentrations of serum C-reactive protein, erythrocyte sedimentation rate, anti-double-stranded DNA (anti-dsDNA) antibody, total lgG, complement 3, and complement 4 were measured. Serum cytokines and chemokines were measured by a cytometric bead array assay. Elevated frequencies of HLA-DR + T cells and ICOS + T cells were observed in SLE patients with positive anti-dsDNA antibodies compared with those in healthy controls ( P 〈 0.001 ). The expression of HLA-DR + T cells was positively correlated with SLEDAI ( r = 0.15 , P 〈 0.01 ). Furthermore, levels of serum IL-6, MCP-1, TNFRI, IL-10, IL-12, and CCL20 were higher in SLE patients compared with healthy controls. In addition, patients with hematologic manifestations displayed elevated frequencies of HLA-DR + T cells and ICOS + T cells. Patients with renal manifestations had a decreased frequency of TIGIT + T cells. These results suggested a dysregulated T cell activity and cytokine expression profiles in SLE subjects. We also developed a chemokine and cytokine profiling strategy to predict the activity of SLE, which has clinical implication for better monitoring the flares and remission during the course of SLE and for assessing therapeutic interventions.
    Type of Medium: Online Resource
    ISSN: 0962-9351 , 1466-1861
    URL: Article
    DOI: 10.1155/2019/8450947
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2019
    detail.hit.zdb_id: 2008065-7
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  • 3
    Online Resource
    Online Resource
    FcγRIIIA Negatively Impacts Humoral Immune Responses but Not Overall Lung Inflammation in an Ovalbumin-Induced Allergic Asthma Mouse Model
    S. Karger AG ; 2018
    In:  International Archives of Allergy and Immunology Vol. 176, No. 1 ( 2018), p. 61-73
    Details
    In: International Archives of Allergy and Immunology, S. Karger AG, Vol. 176, No. 1 ( 2018), p. 61-73
    Abstract: 〈 b 〉 〈 i 〉 Background: 〈 /i 〉 〈 /b 〉 Fcγ receptors (FcγR) play substantial immune regulatory roles both positively and negatively in pathophysiological processes including allergy and asthma. Compared with FcγRIIB which is classically defined as an inhibitory receptor, mouse FcγRIIIA and its functional human homologue FcγRIIA have been assumed to be activating receptors. However, evidence demonstrating inhibitory regulation by mouse FcγRIIIA has recently been emerging. 〈 b 〉 〈 i 〉 Objective: 〈 /i 〉 〈 /b 〉 To dissect the contributory roles of mouse FcγRIIIA (human FcγRIIA) in parallel with FcγRIIB in an ovalbumin (OVA)-induced mouse model of asthma and to preliminarily assess the correlation of the respective FcγR with circulating IgE levels in human asthma patients. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 Wild-type, FcγRIIB 〈 sup 〉 –/– 〈 /sup 〉 , and FcγRIIIA 〈 sup 〉 –/– 〈 /sup 〉 mice were used in an OVA-induced asthma model followed by assessment of the allergic pathology focused on the lung tissues. Expression levels of FcγRIIB, FcγRIIA, and FcγRIIIA on peripheral blood mononuclear cells (PBMC) together with the circulating IgE levels in the serum from patients with allergic asthma were analysed. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Although enhanced humoral immune responses typically represented by augmented OVA-specific IgG and IgE levels in serum were observed in the absence of FcγRIIIA in the mouse asthma model, no overall regulation by FcγRIIIA, especially in terms of those parameters measuring lung tissue inflammation, was recorded. As expected, in the absence of FcγRIIB, augmented immune responses measured as serum antibody levels as well as those in various regulatory pathways in this mouse asthma model were observed. The expression levels of human FcγRIIB but not FcγRIIA were negatively correlated with serum levels of IgE in human asthma patients. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 We did not find major evidence demonstrating an immune inhibitory role of mouse FcγRIIIA in this OVA-induced mouse asthma model. As asthma is a complex disease and the immune regulatory responses involve sophisticated components and pathways, the exact roles of FcγRIIIA as well as its human functional homologue FcγRIIA in asthma still await further clarification using other mouse asthma models as well as clinical studies.
    Type of Medium: Online Resource
    ISSN: 1018-2438 , 1423-0097
    URL: Article
    DOI: 10.1159/000487539
    RVK:
    XA 49650
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482722-0
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