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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.    Electronic supplementary material  The online version of this article (10.1186/s12967-018-1653-x) contains supplementary material, which is available to authorized users.

journal of translational medicine

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