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Autor(en) / Beteiligte
Titel
Mycobacterium tuberculosis Ag85C, MPT51, HspX, and the fusion recombinant CMX proteins or rBCG CMX vaccine modulate the innate immune response in a pro and anti inflammatory manner (VAC9P.1103)
Ist Teil von
  • The Journal of immunology (1950), 2015-05, Vol.194 (1_Supplement), p.145-145.11
Erscheinungsjahr
2015
Link zum Volltext
Quelle
Electronic Journals Library
Beschreibungen/Notizen
  • Abstract Introduction: Mycobacterium tuberculosis produces several proteins that have been associated with its virulence and therefore intensively studied as target for subunit vaccine against tuberculosis. Ag85C, MPT51 and HspX were shown to be immunogenic and antigenic proteins. Also, a fusion protein (rCMX) developed using part of these individual molecules induced specific Th1 and Th17 and poly functional Th cells, that were related to tuberculosis protection. Objectives: This study aimed to understand how this immune response was induced. Methodology: Pulmonary, peritoneal, alveolar, and bone marrow derived macrophages from BALB/c mice were stimulated with the recombinant antigens: Ag85C, MPT51, HspX, CMX or with BCG or rBCG CMX vaccines. Results: All macrophage types responded to Ag85C and CMX with elevated NO production when compared with unstimulated macrophages, while the response to MPT51 and CMX produced urea at similar levels as M2 derived macrophages. HspX did not stimulate macrophages. Pulmonary macrophages infected with BCG produced NO similarly to M1 macrophages, whereas rBCG CMX infection induced urea comparable to M2 macrophages. Conclusion: Ag85C, CMX and MPT51 proteins induced M1, mixed and M2 macrophage phenotypes, respectively. However when CMX was produced within rBCG CMX, a predominant M2 phenotype was observed. The results suggest that the used antigens can modulate the immune response similarly to that shown by rBCG CMX in vivo.
Sprache
Englisch
Identifikatoren
ISSN: 0022-1767
eISSN: 1550-6606
DOI: 10.4049/jimmunol.194.Supp.145.11
Titel-ID: cdi_crossref_primary_10_4049_jimmunol_194_Supp_145_11
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