MHC Polymorphism and Tuberculosis Disease

Mycobacterium tuberculosis (Mtb), the causal agent of tuberculosis (TB), remains a major public health throughout the world causing high mortality in humans. According to the report published by the World Health Organization in 2009, 9.3 million new cases of TB were declared in the world and 1.3 million HIV-negative people died by this infection (http://www.who.int/tb/publications/global_report/2010/en/index.html). One-third of the world’s population is estimated to be infected with Mtb, but, only 1 in 10 subjects who become infected would develop clinical disease. Furthermore, until now it is not fully understood why this category of individuals develop different forms of TB, pulmonary and extra pulmonary TB. Several environmental factors principally malnutrition, HIV infection and a decrease of socio-economic level favours TB progression. Furthermore, it has been confirmed by numerous studies that the outcome of TB infection is under the influence of the host genetic background (Vannberg et al., 2011). In fact, twin studies have revealed the increased concordance of disease in monozygotic compared with dizygotic twins (Jepson et al., 2001; Maartens et al., 2007). In addition, numerous families and case-control studies have demonstrated the involvement of many genes in the control of immune response in the context of the susceptibility or resistance to TB. Among these genes Major Histocompatibility Complex (MHC) takes a substantial and central role in the control of TB infection (Kamath et al., 2004).