**8. Heat shock**

One of the hallmarks of tuberculosis is fever and night sweats in which body temperature increases and is suboptimal for *Mycobacterium tuberculosis* replication and survival. This allows the immune system a competitive edge over the invading microbes. Heat stress can cause damage to *M. tuberculosis* by causing proteins to unfold which may then be degraded. In response, *M. tuberculosis* can upregulate chaperonins which complex with unfolded proteins and help them refold (Table 1.). The α-crystalline protein, or Acr-2, is activated by heat shock, and has demonstrated chaperonin activity (Pang and Howard, 2007).

Many proteins that are upregulated in *M. tuberculosis in vivo* are heat shock proteins that have chaperonine activity. While these proteins may benefit the organism by complexing with and refolding heat damaged proteins, they are also recognized by the immune system. Both the 65Kd heat shock protein and the HSP70 protein can be found extracellularly to *M. tuberculo‐ sis,* and are potent stimulators of an inflammatory response (Anand et al, 2010).
