**6. Role of vitamin D**

Deficiency of vitamin D is associated with higher incidence and manifestation of tuberculosis (Nnoaham KE, 2008; Verway M et al., 2013) and its supplementation helps to overcome this disease. Vitamin D is also able to restore the impaired secretion of TNF-α from macrophages of HIV-positive people (Anandaiah A et al., 2013). It acts as a mediator of innate immune response against M tb by mediating signals from toll like receptors to the activation of antimicrobial peptides (Liu PT et al., 2006). Liu PT et al. 2006, demonstrated that TLR stimu‐ lation by M tb or lipo-polysaccharide activates vitamin D receptors and subsequent down‐ stream signalling activates transcription and translation of cathelicidin, a peptide with antimicrobial properties and thus creating an antimicrobial state in the human macrophages. Vitamin D has a modulatory role on the levels of cytokines specifically IL-1β and thus aid in immunity to the pathogen (Verway M et al., 2013). It also regulates the role of NLRP3/ caspase1 inflammasome leading to regulation of the levels of IL-1β and cross talk between alveolar epithelial cells and macrophages which is required for the synthesis and release of antimicrobial peptides (Verway M et al., 2013).

1, 25-dihydroxyvitamin D3, the active component of vitamin D, plays a major role in induction of autophagy during M tb infections (Yuk JM et al., 2009). This function of vitamin D3 is performed by activation of transcription of Beclin-1 and Atg5 genes and is mediated by cathelicidins (Yuk JM et al., 2009). Vitamin D3 also helps in the formation of autophagosomes, autophagolysosomes and co-localization of M tb cells with them, an important step in the killing of the bacterium (Yuk JM et al., 2009).
