Figure 2.

A hypothetical model explaining the persistence and/or reinfection of Nontuberculosis Mycobacteria (NTM) and the establishment of Mycobacterium bovis bacillus Calmette–Guérin (BCG) vaccine interference. Mouse models clearly indicate that TH1 immunity predominates in situations where this pathogen can be cleared, but there is little evidence, explaining its survival and chronic disease. One hypothesis involves T cell plasticity. The inflammatory Th17 response becomes dominant, resulting in loss of a protective Th1 response and its replacement by cells that can continually drive low-grade inflammation.