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.