Literature DB >> 15870021

Anti-IL-5 and hypereosinophilic syndromes.

Steven A Sutton1, Amal H Assa'ad, Marc E Rothenberg.   

Abstract

Hypereosinophilic syndromes represent a heterogeneous group of disorders characterized by peripheral eosinophilia and end-organ damage associated with eosinophil infiltrations. In many instances, the eosinophilia is refractory to standard therapies and clinicians rely on potentially toxic alternatives. This group of disorders has recently gained attention with the description of patients that harbor a genetic rearrangement that produces a constitutively active tyrosine kinase, often responsive to anti-tyrosine kinase therapy. In addition, the recent expansion in our understanding of the mechanisms by which eosinophils develop and become activated, involving the cytokine interleukin-5 (IL-5), has led to advances in therapeutic options. A new therapy currently in clinical trials is the humanized monoclonal antibody against IL-5. This review will discuss the etiology, classification, and treatment options for the hypereosinophilic syndromes, with particular emphasis on anti-interleukin-5 therapy.

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Year:  2005        PMID: 15870021     DOI: 10.1016/j.clim.2005.02.006

Source DB:  PubMed          Journal:  Clin Immunol        ISSN: 1521-6616            Impact factor:   3.969


  9 in total

1.  The FIP1L1-PDGFRA fusion gene cooperates with IL-5 to induce murine hypereosinophilic syndrome (HES)/chronic eosinophilic leukemia (CEL)-like disease.

Authors:  Yoshiyuki Yamada; Marc E Rothenberg; Andrew W Lee; Hiroko Saito Akei; Eric B Brandt; David A Williams; Jose A Cancelas
Journal:  Blood       Date:  2006-01-17       Impact factor: 22.113

Review 2.  Challenges in addressing the knowledge gap on endomyocardial fibrosis through community-based studies.

Authors:  Jenisse Mbanze; Basilio Cumbane; Rolando Jive; Ana Mocumbi
Journal:  Cardiovasc Diagn Ther       Date:  2020-04

Review 3.  Pharmacokinetics and pharmacodynamics of mepolizumab, an anti-interleukin-5 monoclonal antibody.

Authors:  Deborah A Smith; Elisabeth A Minthorn; Misba Beerahee
Journal:  Clin Pharmacokinet       Date:  2011-04       Impact factor: 6.447

Review 4.  Chemotactic factors associated with eosinophilic gastrointestinal diseases.

Authors:  Carine Blanchard; Marc E Rothenberg
Journal:  Immunol Allergy Clin North Am       Date:  2009-02       Impact factor: 3.479

5.  Clinical problem-solving. The writing on the wall.

Authors:  Brian M Wolpin; Peter F Weller; Joel T Katz; Bruce D Levy; Joseph Loscalzo
Journal:  N Engl J Med       Date:  2009-10-01       Impact factor: 91.245

6.  RNA interference against interleukin-5 attenuates airway inflammation and hyperresponsiveness in an asthma model.

Authors:  Shao-xing Chen; Feng-ying Huang; Guang-hong Tan; Cai-chun Wang; Yong-hao Huang; Hua Wang; Song-lin Zhou; Fan Chen; Ying-ying Lin; Jun-bao Liu
Journal:  J Zhejiang Univ Sci B       Date:  2009-01       Impact factor: 3.066

Review 7.  Hypereosinophilic syndromes.

Authors:  Florence E Roufosse; Michel Goldman; Elie Cogan
Journal:  Orphanet J Rare Dis       Date:  2007-09-11       Impact factor: 4.123

8.  Effectiveness of a combination of cyclosporine A, suplatast tosilate and prednisolone on periodic oscillating hypereosinophilia.

Authors:  Shinsaku Imashuku; Ikuyo Ueda; Tohru Inaba
Journal:  Int Med Case Rep J       Date:  2011-11-08

9.  JAK2-centered interactome hotspot identified by an integrative network algorithm in acute Stanford type A aortic dissection.

Authors:  Sun Pan; Duojiao Wu; Andrew E Teschendorff; Tao Hong; Linyan Wang; Mengjia Qian; Chunsheng Wang; Xiangdong Wang
Journal:  PLoS One       Date:  2014-02-24       Impact factor: 3.240

  9 in total

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