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CTLA4-IgG reverses asthma manifestations in a mild but not in a more "severe" ongoing murine model.

Authors: Deurloo, DT  Van Esch, BC  Hofstra, CL  Nijkamp, FP  Van Oosterhout, AJ 
Citation: Deurloo DT, etal., Am J Respir Cell Mol Biol. 2001 Dec;25(6):751-60.
Pubmed: (View Article at PubMed) PMID:11726402
DOI: Full-text: DOI:10.1165/ajrcmb.25.6.4607

We investigated whether CTLA4-Ig can reverse established asthma manifestations in a novel murine model of ongoing disease. In BALB/c mice, sensitized to ovalbumin (OVA) without adjuvant, airway inflammation was induced by a first series of OVA aerosol challenges. Murine CTLA4-IgG was then administered, followed by a second series of OVA inhalations. In control-treated mice, two series of OVA challenges induced upregulation of OVA-specific IgE in serum, eosinophils in the bronchoalveolar lavage fluid (BALF), and IL-5 production by lung lymphocytes upon OVA restimulation in vitro, compared with saline-challenged mice. CTLA4-IgG significantly inhibited all of these parameters in OVA-challenged mice. Importantly, mCTLA4-IgG performed better than the gold-standard dexamethasone because this corticosteroid did not inhibit the upregulation of OVA-specific IgE in serum. In a more "severe" ongoing model, induced by sensitization to OVA emulsified in aluminum hydroxide, resulting in airway hyperresponsiveness to methacholine and stronger inflammatory responses, mCTLA4-IgG was less effective in that only the number of eosinophils in the BALF was reduced (P = 0.053), whereas dexamethasone inhibited both BALF eosinophilia and cytokine production by lung lymphocytes. Thus, CTLA4-Ig might be an effective alternative therapy in established allergic asthma, especially in situations of mild disease.

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CRRD Object Information
CRRD ID: 11344922
Created: 2016-07-08
Species: All species
Last Modified: 2016-07-08
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.