The scourge of tuberculosis is continuing to toll around 1.5 million human lives annually. The only vaccine against tuberculosis is BCG which gives varied protection in various regions and races of the world. Developing new vaccine based on mycobacterial strains is a challenging task given the fact that the majority of population living near tropics carries varying degree of tolerance against either BCG or Non-Tuberculous Mycobacteria (NTM). Moreover, the fact that ≈90% of Mycobacterium tuberculosis (Mtb) infected population restrain the bacilli on its own; strengthen the case for harnessing the power of host’s own immune system to advance the protective efficacy of mycobacterial vaccines. In general, Mtb modulates IL-10/STAT3 signaling to skew host mononuclear phagocytes towards alternatively activated, anti-inflammatory state. The as-generated anti-inflammatory ambience helps Mtb to thrive against hostile immune advances. We thus hypothesized that modulating IL-10/STAT3 driven anti-inflammatory effects, may improve the prophylactic ability of vaccines against tuberculosis. Here, we investigated the immunotherapeutic ability of a porphyrin analogue, 5,15-diphenyl porphyrin (DPP), to improve anti-TB immunity offered by 2nd generation recombinant BCG30 (rBCG30-ARMF-II®) vaccine. The DPP therapy potentiated vaccine induced anti-TB immunity by down-modulating anti-inflammatory responses driven via engagement of IL-10/10R and subsequent STAT3 activation. The employed immunotherapy with DPP conferred augmented resistance to aerosol Mtb challenge in BALB/c mice. The protection was accompanied with predominant early proliferation of pro-inflammatory monocytes/macrophages/DCs, enhanced expansion of CD4+ and CD8+ central memory T cells and dynamic equilibrium between amplification of Th17 and Treg cells.