| Autor: |
Alberca Custodio RW; Institute of Biomedical Sciences, Department of Immunology, University of Sao Paulo, Sao Paulo 05508-000, Brazil. Ricardowesley@gmail.com., Mirotti L; Institute of Biomedical Sciences, Department of Immunology, University of Sao Paulo, Sao Paulo 05508-000, Brazil. lmirotti@gmail.com., Gomes E; Institute of Biomedical Sciences, Department of Immunology, University of Sao Paulo, Sao Paulo 05508-000, Brazil. melloeag@gmail.com., Nunes FPB; Institute of Biomedical Sciences, Department of Immunology, University of Sao Paulo, Sao Paulo 05508-000, Brazil., S Vieira R; Institute of Biomedical Sciences, Department of Immunology, University of Sao Paulo, Sao Paulo 05508-000, Brazil. raqueldesouzavieira@outlook.com., Graça L; Institute of Molecular Medicine, University of Lisbon, 1649-028 Lisbon, Portugal. lgraca@medicina.ulisboa.pt., R Almeida R; Institute of Biomedical Sciences, Department of Immunology, University of Sao Paulo, Sao Paulo 05508-000, Brazil. rafaelbio13@yahoo.com.br., S Câmara NO; Institute of Biomedical Sciences, Department of Immunology, University of Sao Paulo, Sao Paulo 05508-000, Brazil. niels@icb.usp.br., Russo M; Institute of Biomedical Sciences, Department of Immunology, University of Sao Paulo, Sao Paulo 05508-000, Brazil. momrusso@usp.br. |
| Abstrakt: |
Elevated levels of immunoglobulin E (IgE) are associated with allergies and other immunological disorders. Sensitization with alum adjuvant favours IgE production while CpG-ODN adjuvant, a synthetic toll-like receptor 9 (TLR9) agonist, inhibits it. The cellular mechanisms underlying in vivo TLR regulation of immunoglobulin production, specially IgE, are still controversial. Specifically, TLR-mediated IgE regulation in vivo is not yet known. In this study we showed that augmented levels of IgE induced by sensitizations to OVA with or without alum adjuvant or with OVA-pulsed dendritic cells (DCs) were inhibited by co-administration of CpG. Notably, CpG-mediated suppression of IgE production required MyD88 -expression on DCs but not on B-cells. This finding contrasts with previous in vitro studies reporting regulation of IgE by a direct action of CpG on B cells via MyD88 pathway. In addition, we showed that CpG also inhibited IgE production in a MyD88 -dependent manner when sensitization was performed with OVA-pulsed DCs. Finally, CpG signalling through MyD88 pathway was also necessary and sufficient to prevent anaphylactic antibody production involved in active cutaneous anaphylaxis. |
