For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
13
views
65
references
 Top references
cited by
17
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      395
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Anti-IgE therapy for IgE-mediated allergic diseases: from neutralizing IgE antibodies to eliminating IgE + B cells

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Allergic diseases are inflammatory disorders that involve many types of cells and factors, including allergens, immunoglobulin (Ig)E, mast cells, basophils, cytokines and soluble mediators. Among them, IgE plays a vital role in the development of acute allergic reactions and chronic inflammatory allergic diseases, making its control particularly important in the treatment of IgE-mediated allergic diseases. This review provides an overview of the current state of IgE targeted therapy development, focusing on three areas of translational research: IgE neutralization in blood; IgE-effector cell elimination; and IgE + B cell reduction. IgE-targeted medicines such as FDA approved drug Xolair (Omalizumab) represent a promising avenue for treating IgE-mediated allergic diseases given the pernicious role of IgE in disease progression. Additionally, targeted therapy for IgE-mediated allergic diseases may be advanced through cellular treatments, including the modification of effector cells.

          Related collections

          Most cited references65

          • Record: found
          • Abstract: found
          • Article: not found

          The role of the mast cell in the pathophysiology of asthma.

          Peter Bradding, Andrew F. Walls, Stephen T. Holgate (2006)
          There is compelling evidence that human mast cells contribute to the pathophysiology of asthma. Mast cells, but not T cells or eosinophils, localize within the bronchial smooth muscle bundles in patients with asthma but not in normal subjects or those with eosinophilic bronchitis, a factor likely to be important in determining the asthmatic phenotype. The mechanism of mast cell recruitment by asthmatic airway smooth muscle involves the CXCL10/CXCR3 axis, and several mast cell mediators have profound effects on airway smooth muscle function. The autacoids are established as potent bronchoconstrictors, whereas the proteases tryptase and chymase are being demonstrated to have a range of actions consistent with key roles in inflammation, tissue remodeling, and bronchial hyperresponsiveness. IL-4 and IL-13, known mast cell products, also induce bronchial hyperresponsiveness in the mouse independent of the inflammatory response and enhance the magnitude of agonist-induced intracellular Ca2+ responses in cultured human airway smooth muscle. There are therefore many pathways by which the close approximation of mast cells with airway smooth muscle cells might lead to disordered airway smooth muscle function. Mast cells also infiltrate the airway mucous glands in subjects with asthma, showing features of degranulation, and a positive correlation with the degree of mucus obstructing the airway lumen, suggesting that mast cells play an important role in regulating mucous gland secretion. The development of potent and specific inhibitors of mast cell secretion, which remain active when administered long-term to asthmatic airways, should offer a novel approach to the treatment of asthma.
          Article 0 comments Cited 121 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Efficacy and safety of a recombinant anti-immunoglobulin E antibody (omalizumab) in severe allergic asthma.

            S Holgate, A Chuchalin, J. Hebert … (2004)
            Patients with severe asthma are often inadequately controlled on existing anti-asthma therapy, constituting an unmet clinical need. This randomized, double-blind, placebo-controlled trial evaluated the ability of omalizumab, a humanized monoclonal anti-IgE antibody, to improve disease control sufficiently to enable inhaled corticosteroid reduction in patients with severe allergic asthma. After a run-in period when an optimized fluticasone dose (> or =1000 microg/day) was received for 4 weeks, patients were randomized to receive subcutaneous omalizumab [minimum 0.016 mg/kg/IgE (IU/mL) per 4 weeks; n=126] or matching placebo (n=120) at intervals of 2 or 4 weeks. The study comprised a 16-week add-on phase of treatment followed by a 16-week fluticasone-reduction phase. Short-/long-acting beta(2)-agonists were allowed as needed. Median reductions in fluticasone dose were significantly greater with omalizumab than placebo: 60% vs. 50% (P=0.003). Some 73.8% and 50.8% of patients, respectively, achieved a > or =50% dose reduction (P=0.001). Fluticasone dose reduction to < or =500 microg/day occurred in 60.3% of omalizumab recipients vs. 45.8% of placebo-treated patients (P=0.026). Through both phases, omalizumab reduced rescue medication requirements, improved asthma symptoms and asthma-related quality of life compared to placebo. Omalizumab treatment improves asthma control in severely allergic asthmatics, reducing inhaled corticosteroid requirements without worsening of symptom control or increase in rescue medication use.
            Article 0 comments Cited 93 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Celastrol, a novel triterpene, potentiates TNF-induced apoptosis and suppresses invasion of tumor cells by inhibiting NF-kappaB-regulated gene products and TAK1-mediated NF-kappaB activation.

              Krishna Pandey, Bharat B. Aggarwal, Gautam Sethi … (2007)
              Celastrol, a quinone methide triterpene derived from the medicinal plant Tripterygium wilfordii, has been used to treat chronic inflammatory and autoimmune diseases, but its mechanism is not well understood. Therefore, we investigated the effects of celastrol on cellular responses activated by TNF, a potent proinflammatory cytokine. Celastrol potentiated the apoptosis induced by TNF and chemotherapeutic agents and inhibited invasion, both regulated by NF-kappaB activation. We found that TNF induced the expression of gene products involved in antiapoptosis (IAP1, IAP2, Bcl-2, Bcl-XL, c-FLIP, and survivin), proliferation (cyclin D1 and COX-2), invasion (MMP-9), and angiogenesis (VEGF) and that celastrol treatment suppressed their expression. Because these gene products are regulated by NF-kappaB, we postulated that celastrol mediates its effects by modulating the NF-kappaB pathway. We found that celastrol suppressed both inducible and constitutive NF-kappaB activation. Celastrol was found to inhibit the TNF-induced activation of IkappaBalpha kinase, IkappaBalpha phosphorylation, IkappaBalpha degradation, p65 nuclear translocation and phosphorylation, and NF-kappaB-mediated reporter gene expression. Recent studies indicate that TNF-induced IKK activation requires activation of TAK1, and we indeed found that celastrol inhibited the TAK1-induced NF-kappaB activation. Overall, our results suggest that celastrol potentiates TNF-induced apoptosis and inhibits invasion through suppression of the NF-kappaB pathway.
              Article 0 comments Cited 73 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Jiayun Hu: hujiayun11@126.com
                Jiajie Chen: tieniu03@126.com
                Lanlan Ye: 782053751@qq.com
                Zelang Cai: 175587278@qq.com
                Jinlu Sun: +86-755-86671979 , sunjinlv@pumch.cn
                Kunmei Ji: +86-755-86671979 , jkm@szu.edu.cn
                Journal
                Journal ID (nlm-ta): Clin Transl Allergy
                Journal ID (iso-abbrev): Clin Transl Allergy
                Title: Clinical and Translational Allergy
                Publisher: BioMed Central (London )
                ISSN (Electronic): 2045-7022
                Publication date (Electronic): 18 July 2018
                Publication date PMC-release: 18 July 2018
                Publication date Collection: 2018
                Volume: 8
                Electronic Location Identifier: 27
                Affiliations
                [1 ]ISNI 0000 0001 0472 9649, GRID grid.263488.3, Department of Biochemistry and Molecular Biology, , School of Medicine of Shenzhen University, ; Shenzhen, 518035 China
                [2 ]ISNI 0000 0001 0662 3178, GRID grid.12527.33, Department of Allergy, Peking Union Medical College Hospital, , Peking Union Medical College and Chinese Academy of Medical Sciences, ; Beijing, 100730 China
                Article
                Publisher ID: 213
                DOI: 10.1186/s13601-018-0213-z
                PMC ID: 6050685
                PubMed ID: 30026908
                SO-VID: 08fc8f62-d53b-4952-ad44-f956e1aac8c7
                Copyright © © The Author(s) 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 9 April 2018
                Date accepted : 28 May 2018
                Funding
                Funded by: NSFC
                Award ID: 81571570
                Award Recipient :
                Funded by: CAMS Innovation Fund for Medical Sciences
                Award ID: CIFMS: 2016-I2M-1003
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Immunology
                Keywords: anti-ige therapy,allergic diseases,ige+ b cells,ige neutralization
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: anti-ige therapy, allergic diseases, ige+ b cells, ige neutralization

                Comments

                Comment on this article

                scite_

                Similar content395

                See all similar

                Cited by17

                See all cited by

                Most referenced authors931

                See all reference authors