**4. Inflammasomes in tuberculosis**

As briefly discussed above inflammasomes play a regulatory role in tuberculosis and imparts protection if activated. For its survival M tb prevents the activation of inflammasomes, caspase-1 dependent processing of pro-IL-1β and phagosome maturation through its gene zmp1 (Master SS et al., 2008; Lazarevic V and Martinon F, 2008). It has been shown that the production of IL-1β is dependent on the recognition of M tb by pattern recognition receptors (PRR) TLR2/TLR6 and NOD2 (Kleinnijenhuis J et al., 2009). TLR4, the other PRR which is important in M tb recognition does not play major role in production of IL-1β. The immune adaptor molecule MyD88 has a central role in the transcription of the IL-1β mRNA during M tb infection (Kleinnijenhuis J et al., 2009).

Absence in melanoma 2 (AIM2) inflammasome is a cytosolic sensor of the DNA and recognises DNA viruses and intracellular bacteria. Co-localisation of M tb DNA with AIM2 inflamma‐ some has been observed suggesting their direct interaction (Saiga H et al., 2012). AIM2 inflammasomes are involved in activation of macrophages and secretion of IL-1β during infection with pathogenic strain of *Mycobacterium bovis* suggesting its co-operative role in host immunity (Yang Y, 2013). AIM2 deficient mice are more susceptible to M tb infection and are defective in production of IL-1β and IL-18 and mount poor Th1 response (Saiga H et al., 2012). These authors also speculated on the role of AIM2 inflammasome in suppressing type I interferons in M tb infections. NLRP3 inflammasome is implicated in the protective immune response to M tb infection by facilitating the maturation process of IL-1β (Rathinam VA et al., 2012). However, M tb suppresses the activation of the NLRP3 inflammasome by inducing IFNβ, while IFN-β induces the AIM2 inflammasome which is detrimental to the pathogen (Fernandes-Alnemri T et al., 2010; Tsuchiya K et al. 2010; Briken V et al., 2013). Thus M tb balances the level of IFN-β such that NLRP3 inflammasome is kept suppressed and the AIM2 inflammasome is not allowed to be activated. This is done by the ESX-1 secretion system which is dependent on the ESAT6-an RD1 region encoded protein of M tb (Shah S et al., 2013).

Activating inflammasomes, although critical for protection from M tb infection and tubercu‐ losis, also need to be regulated to prevent the tissue damage and rampant inflammation. Host regulation of NLRP3 inflammasome is done by nitric oxide which acts as its negative regulator during M tb infection and consequently controls the level of IL-1β (Mishra BB. et al., 2013).
