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    A lipidated bi-epitope vaccine comprising of MHC-I and MHC-II binder peptides elicits protective CD4 T cell and CD8 T cell immunity against Mycobacterium tuberculosis

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    Author
    Rai, PK; Chodisetti, SB; Maurya, SK; Nadeem, S; Zeng, W; Janmeja, AK; Jackson, DC; Agrewala, JN
    Date
    2018-10-11
    Source Title
    Journal of Translational Medicine
    Publisher
    BMC
    University of Melbourne Author/s
    Zeng, Weiguang; Jackson, David
    Affiliation
    Microbiology and Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    Rai, P. K., Chodisetti, S. B., Maurya, S. K., Nadeem, S., Zeng, W., Janmeja, A. K., Jackson, D. C. & Agrewala, J. N. (2018). A lipidated bi-epitope vaccine comprising of MHC-I and MHC-II binder peptides elicits protective CD4 T cell and CD8 T cell immunity against Mycobacterium tuberculosis. JOURNAL OF TRANSLATIONAL MEDICINE, 16 (1), https://doi.org/10.1186/s12967-018-1653-x.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/253233
    DOI
    10.1186/s12967-018-1653-x
    Abstract
    BACKGROUND: The clinical trials conducted at Chingleput India suggest that BCG fails to protect against tuberculosis (TB) in TB-endemic population. Recent studies advocate that non-tuberculous mycobacteria and latent Mycobacterium tuberculosis (Mtb) infection interferes in the antigen processing and presentation of BCG in inducing protective immunity against Mtb. Thereby, indicating that any vaccine that require extensive antigen processing may not be efficacious in TB-endemic zones. Recently, we have demonstrated that the vaccine candidate L91, which is composed of lipidated promiscuous MHC-II binder epitope, derived from latency associated Acr1 antigen of Mtb is immunogenic in the murine and Guinea pig models of TB and conferred better protection than BCG against Mtb. METHODS: In this study, we have used a multi-stage based bi-epitope vaccine, namely L4.8, comprising of MHC-I and MHC-II binding peptides of active (TB10.4) and latent (Acr1) stages of Mtb antigens, respectively. These peptides were conjugated to the TLR-2 agonist Pam2Cys. RESULTS: L4.8 significantly elicited both CD8 T cells and CD4 T cells immunity, as evidenced by increase in the enduring polyfunctional CD8 T cells and CD4 T cells. L4.8 efficiently declined Mtb-burden and protected animals better than BCG and L91, even at the late stage of Mtb infection. CONCLUSIONS: The BCG-L4.8 prime boost strategy imparts a better protection against TB than the BCG alone. This study emphatically denotes that L4.8 can be a promising future vaccine candidate for controlling active and latent TB.

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