J allergy clin immunol impact factor 8 5

10.01.2020| Marquis Mclain| 0 comments

j allergy clin immunol impact factor 8 5

The accumulation of dust mite allergens on mattresses made of different kinds of materials. Asian Pac J Allergy Immunol ; Mahakittikun V, Boitano JJ. Research and innovation on house dust mites. Siriraj Medical Journal ;
  • Seminars in Immunology
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  • Regulating Bcl2L12 expression in mast cells inhibits food allergy
  • The p53 protein repairs damaged cells clin induces apoptosis in those that cannot be repaired. The factor gene transcriptome of mast cells was then analyzed. We found that the B cell lymphoma protein 2 like 12 protein Immunol was unusually active Figure. S1 in Supplemental Materials.

    Published data also indicate that Bcl2L12 plays a critical role in anti-apoptotic machinery development. Early reports indicated that Bcl2L12 played a role in the anti-apoptotic feature of glioma cells, as wells as impact other cancers [ 13 ]. Later studies showed that Bcl2L12 was expressed in other cell types, such as liver cells [ 14 ], cardiovascular endothelial cells [ 15 ] and immune cells [ 16 ] [ 17 allergy.

    Whether Bcl2L12 is associated with the aberrant regulation of mast cell activities e. Allergic reactions activate mast cells.

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    Allergic diseases are the result of hyperresponsiveness of the body immune system to innocent antigens, including allergic asthma, allergic rhinitis, allergic dermatitis and food allergy FA.

    The immune system produces specific IgE antibodies against specific antigens. Re-exposure to specific antigens triggers sensitized mast cells to release chemical mediators to evoke allergic reactions [ 18 ]. Cumulative reports indicate that the number of mast cells in the tissues with allergic disorders allergy markedly increased compared to normal tissues [ 18 factor. Based on the information above, we hypothesize clin the apoptosis machinery in the mast cells of subjects with allergic disorders is impaired.

    To test the hypothesis, an FA mouse model was developed, and the activation-induced mast cell apoptosis in the FA mouse intestinal tissue was characterized.

    The mice were maintained in a specific pathogen-free facility with accessing water and food freely. The animal experimental procedures used in the present study were approved by the Animal Ethics Committee at Shenzhen University.

    To test the allergy status in the intestine, following items immunol examined:. Impact of mast cells in lamina propria mononuclear cells LPMC.

    Levels of Th1 and Th2 cytokines in extracts of intestinal tissue. The core temperature changes upon challenge with specific antigens. Intestinal segments were snap frozen in liquid nitrogen. The sections were observed with a fluorescent microscope. The number of mast cells was counted in 20 randomly selected windows, which were averaged as one datum. The sections were coded.

    The observers were not aware of the code to avoid the observer bias. LPMCs were prepared as described above. Mast cells were purified from LPMCs by flow cytometry cell sorting. The culture medium, including the reagents, was changed in every 3 days.

    The mice were sacrificed next day. The results of transfection were checked by Western blotting 48 h after. The difference between two groups was determined by Student t test. If necessary, the Pearson correlation assay was performed between two parameters of interest. The mice were sacrificed the next day.

    The cells were analyzed with a flow cytometer. About 1. Further analysis showed that about The data were verified by immunohistochemistry analysis, and about The results indicate that mast cells in the FA mouse intestine have apoptosis defects. Because p53 is also involved in mast cell apoptosis [ 22 ], we assessed the expression of p53 in mast cells. The results suggest that the suppression of the FasL expression may be associated with the apoptosis defects of mast cells in FA mice. Since FasL can be produced by other cell types, such as T cells [ 23 ], whether exogenous FasL can induce mast cell apoptosis is unclear.

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    Mast cells in the intestine of FA mice show apoptosis defects. The cells were analyzed by flow cytometry. A, gated dot plots facto frequency of mast cells.

    B, bars indicate summarized data of the gated dot plots in panel A. C, gated histograms indicate apoptotic mast cells in LPMC.

    D, bars indicate frequency of apoptotic mast cells in LPMCs.

    J Allergy Clin Immunol. Jun;(6) doi: /sbkt.alexeevphoto.ru Epub Nov 8. Biallelic interferon regulatory factor 8 mutation: A complex immunodeficiency syndrome with dendritic cell deficiency, monocytopenia, and immune sbkt.alexeevphoto.ru by: Journal description. Clinical and Diagnostic Laboratory Immunology publishes peer-reviewed articles, minireviews, case reports, and guest commentaries on a variety of topics related to clinical. Journal Impact Factor (IF) is a measure reflecting the average number of citations to articles published in science and social science journals. It is frequently used as a proxy for the relative importance of a journal within its field, with journals with higher impact factors deemed to be more important than those with lower ones. via Wikipedia.

    E, bars indicate serum levels of mMCP1. F, representative images show factor in green mast cells in red in mouse intestine.

    G, bars show frequency of apoptotic mast cells. Each c,in inside bars presents data from an independent experiment. FA suppresses activation-induced FasL expression in mast cells. E, levels of p53 clin in mast cells. To investigate the role of Th2 polarization in inducing apoptosis defects in mast cells, we collected intestinal samples from FA and control mice. Protein extracts were prepared. The results suggest that IL-5 may be associated immuno, the lower expression of FasL in impact cells of FA mouse intestine.

    Because Bcl2L12 plays a role in inducing an anti-apoptotic feature in cancer cells imumnol 13 ], we sought to determine whether Bcl2L12 alledgy also involved in inducing apoptotic defects in mast cells. Data in Figure 5 indicate that Bcl2L12 induces apoptosis defects in mast allergy, suggesting that inhibiting Bcl2L12 may immunol the apoptosis machinery in mast cells of FA subjects.

    LPMCs were isolated from mice and analyzed by flow cytometry. Mast cells were counted in the intestinal tissue by immunohistochemistry. The results demonstrate that inhibition of Bcl2L12 can restore the apoptotic machinery in mast cells of FA mice, which efficiently attenuates FA response.

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    Intestinal mast cells were isolated by MACS. Gated dot plots indicate clun of apoptotic mast cells. Bars indicate summarized data of apoptotic mast cells. Each dot represent data from one mouse.

    IL-5 suppresses FasL expression in mast cells. BMMCs were treated with procedures denoted above each dot plot panel. A, gated dot plots show frequency of apoptotic BMMCs.

    Journal Impact Factor (IF) is a measure reflecting the average number of citations to articles published in science and social science journals. It is frequently used as a proxy for the relative importance of a journal within its field, with journals with higher impact factors deemed to be more important than those with lower ones. via Wikipedia. Journal description. Clinical and Diagnostic Laboratory Immunology publishes peer-reviewed articles, minireviews, case reports, and guest commentaries on a variety of topics related to clinical. Systemic mastocytosis and senior age are major, unmodifiable long‐term risk factors and thus reinforce the indication for venom immunotherapy. Vespid venom allergy and male sex likewise augment the risk of severe or even fatal reactions. Further studies are required to assess the impact of specific cardiovascular sbkt.alexeevphoto.ru: Johanna Stoevesandt, Gunter J. Sturm, Patrizia Bonadonna, Joanna N.G. Oude Elberink, Axel Trautmann.

    Bars show summarized apoptotic cells. Each dot represent data from one experiment. We observed that apoptosis could be induced in mast cells after activation in physiological conditions, but not in an allergic environment. IL-5, one of the Th2 cytokines, increased the expression of Bcl2L12 in mast cells.

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    Bcl2L12 formed a complex with c-Myc, the transcription factor of FasL, in mast cells to restrict the expression of FasL.

    Inhibition of Bcl2L12 restored the apoptosis machinery in mast cells of Impxct mice and attenuated mast cell-related FA aklergy. Mast cells play a critical role in the pathogenesis of allergic inflammation and other types of chronic inflammation, such as inflammatory bowel disease [ 26 ].

    Mast cells also have physiological functions—that is, they help to cure of wounds, expel pathogens, etc. Mast cells express Toll like receptors TLR [ 27 ] that can recognize the stimuli of pathogens, including parasites, bacteria and viruses.

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    In other words, mast cells can be activated by exposure to pathogens. Once activated, mast cells release many chemical mediators to expel the invaded pathogens [ 28 ].

    This phenomenon demonstrates that apoptosis can be triggered in mast cells after activation to terminate the release of chemical mediators to avoid inducing tissue injury and inflammation.

    j allergy clin immunol impact factor 8 5

    Bcl2L12 suppresses FasL expression in mast cells. Immunoblots indicate Bcl2L12 levels. Each dot represent data from one mouse or one experiment. The data show that exposure to IL-5, one of the Th2 cytokines, prevents the induction of apoptosis in mast cells by inducing the expression of Bcl2L Over production of Th2 cytokines is one of the features of allergic diseases and some other inflammations [ factor ].

    IL-5 is the key cytokine to promote the development of eosinophils [ 30 ]. The present data add novel information to the characteristics of IL-5; IL-5 not only regulates eosinophil development, but it also regulates mast cell activities by inducing the expression of Bcl2L12 in mast cells.

    Previous studies show that mast cells express FasL [ 11 ]. Our data are in line with the data; we also found that intestinal mast cells and BMMCs expressed FasL, which could be up regulated by activation. The present study has revealed a novel factor, Bcl2L12, in the suppression of apoptosis in mast cells factor regulating the expression of FasL at gene transcription levels. Inhibition of Bcl2L12 restores apoptosis machinery in mast cells of FA mice. LPMCs allergy prepared and analyzed by immunol cytometry.

    A, gated dots indicate frequency of mast cells in LPMCs. B, bars indicate summarized mast cell frequency in LPMCs. C, gated histograms indicate apoptotic mast cells in LPMCs. D, bars indicate summarized apoptotic mast cells in LPMCs. G, bars indicate mast cell counts in the intestinal mucosa representative images are presented impact Fig S6. H, bars indicate serum levels of mMCP1. Blood samples were collected. Bcl2L12 is a member of the anti-apoptotic family.

    By suppressing p53 protein, caspase 3 and caspase 7, Bcl2L12 exerts its role of anti-apoptosis. Early studies found that Allergy was mainly involved in the pathogenesis of cancers [ 13 ]. Later, it was found that Bcl2L12 was immunol associated with activities of other cell types [ 1415 ]. Clin previous studies found that Bcl2L12 was involved in immune deregulation by interfering with the expression of IL in peripheral B cells of patients with allergic rhinitis [ 16 ] impact inflammatory bowel disease [ 32 ] and facilitating the development of Th2 polarization [ 17 ].

    The present data add novel information to the pathogenesis of disorders with mast cells—that is, IL-5 and Bcl2L12 play a role in the development and maintenance of mast cell over population in clin local tissue.

    It is noteworthy that Bcl2L12 KO mice still have mast cells in the intestine in similar amounts compared with WT mice, indicating that Bcl2L12 is not involved in the lineage development of mast cells. Mast cells are the main effector pro-inflammatory cells in allergic diseases. By releasing chemical mediators, mast cells induce an allergic response and inflammation in the local tissue or induce systemic response such as anaphylaxis [ 1 ].

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    Regulating Bcl2L12 expression in mast cells inhibits food allergy

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