{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,18]],"date-time":"2026-06-18T15:24:14Z","timestamp":1781796254453,"version":"3.54.5"},"reference-count":34,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2015,8,24]],"date-time":"2015-08-24T00:00:00Z","timestamp":1440374400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2015,9]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Allergic asthma is a chronic pulmonary disease characterized by a Th2 inflammatory response. The modulation of a Th2 immune response based on immune deviation to a Th1 pattern or induction and migration of regulatory T cells to the lungs constitutes one of the major therapeutic approaches that is being investigated for the treatment of allergic asthma. The potentials of <jats:italic>Mycobacterium leprae<\/jats:italic> 65\u2010<jats:styled-content style=\"fixed-case\">kD<\/jats:styled-content> heat\u2010shock protein or Toll\u2010like receptor 9 ligand (CpG oligodeoxynucleotides) as immune modulators for the treatment of airway allergic disease have been studied individually.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>Mycobacterial protein combined with CpG was used as immunotherapy for airway allergy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Using an ovalbumin\u2010induced asthma model, mice were sensitized and challenged, and then treated with mycobacterial heat\u2010shock protein (Hsp65) combined with CpG.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The treatment of mice with established allergy led to the attenuation of eosinophilia, Th2 cytokines and airway hyperresponsiveness. Hsp65 plus CpG treatment also induced an increase in <jats:styled-content style=\"fixed-case\">OVA<\/jats:styled-content>\u2010specific <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 levels and in the frequency of lung inflammatory monocytes. Moreover, we show that the reduction of eosinophilia and the recruitment of inflammatory monocytes to the lungs required early triggering of <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>9, <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3 and <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>2 by immunotherapy components.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>In addition to immune deviation to a Th1 response in the modulation of Th2 allergic inflammation, our findings also attribute an important role to the innate response mediated by <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>9, associated with the recruitment of <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>2\u2010dependent monocytes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Clinical Relevance<\/jats:title><jats:p>Our findings show that the Hsp65\/CpG treatment is a promising strategy for consideration in translational studies.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cea.12564","type":"journal-article","created":{"date-parts":[[2015,5,5]],"date-time":"2015-05-05T15:27:46Z","timestamp":1430839666000},"page":"1459-1471","source":"Crossref","is-referenced-by-count":18,"title":["Attenuation of experimental asthma by mycobacterial protein combined with CpG requires a <scp>TLR<\/scp>9\u2010dependent <scp>IFN<\/scp>\u2010\u03b3\u2010<scp>CCR<\/scp>2 signalling circuit"],"prefix":"10.1111","volume":"45","author":[{"given":"R. Q.","family":"Prado","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Immunology Ribeir\u00e3o Preto Medical School University of S\u00e3o Paulo Ribeir\u00e3o Preto Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T. B.","family":"Bertolini","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Immunology Ribeir\u00e3o Preto Medical School University of S\u00e3o Paulo Ribeir\u00e3o Preto Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. R.","family":"Pi\u00f1eros","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Immunology Ribeir\u00e3o Preto Medical School University of S\u00e3o Paulo Ribeir\u00e3o Preto Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. F.","family":"Gembre","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Immunology Ribeir\u00e3o Preto Medical School University of S\u00e3o Paulo Ribeir\u00e3o Preto Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. G.","family":"Ramos","sequence":"additional","affiliation":[{"name":"Department of Pathology Ribeir\u00e3o Preto Medical School University of S\u00e3o Paulo Ribeir\u00e3o Preto Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. L.","family":"Silva","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Immunology Ribeir\u00e3o Preto Medical School University of S\u00e3o Paulo Ribeir\u00e3o Preto Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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