Figure 2: A diagrammatic model which highlights the difference in Treg suppression in healthy and latently infected individuals and active TB subjects in context of expansion of HLA-DR+CD4+ memory T cells.Individuals infected with TB can either clear the bacteria, become latently infected or come down with active TB disease. There is also a possibility of reactivation of TB in latently infected subjects. The reasons for this can be HIV co-infection, treatment with check-point inhibitors like anti-PD-1, therapies such as anti-TNF for rheumatoid arthritis etc. HLA-DR+ activated cells are low in healthy and latently infected individuals and Treg suppression is good. However, in active TB, HLA-DR+CD4+ T cells expand and Treg mediated suppression becomes poor. The Treg suppression pathways that are rendered inactive in TB are the PD-1/PD-L1 and β-chemokine-CCR5 dependent. The reason for their becoming inactive could be possible counter-regulation by IL-2, IL-17A, IFNγ, IL-22 that are secreted by the expanded HLA-DR+CD4+ T cells.