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Ni L et al
demonstrated high levels of PD-1 expressions on Tregs
in in the peripheral blood of subjects with 
hepatitis C virus lymphoma ( HCV-L) compared to non-HCV-L and blocking
of PD1-PDL1 pathway  reduced the number
of Tregs and suppressed T-cell activation and proliferation in HCV-L was
partially restored.14

   We also found that   expression
of PD1 on CD4+  T-cells and its ligands(PD-L1)
in monocytes  were much higher in APTBs
patients , which was in accordance with results of study done by Shen L
et al.4 Increased expression
of PD1 on CD4+CD25+Foxp3+ than in CD4+CD25+
Foxp3- T-cells is also consistent with reports done by Alexander SA et al and Asano T et.12,13

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  Collectively our findings   apparently   indicate that,  a dynamic imbalance between proportion
of  T-cell subpopulations  follow 
in M.tb infection and  conversion  of T-helper cells  to negative sub-populations severely impaired
cell mediated immunity and contributed to development of active tuberculosis
and PD1-PDL1  has a role in conversion
and maintenance of Treg in active pulmonary tuberculosis .

There are several limitatons to the present study. First, the number of
cases was small. Second during the selection of latently infected individuals,
we did not consider the nutritional level of study subjects which may influence
the IGRA and montoux test and may give false negative results. Third, we did
not correlate the changes in functional phenotypes of T-helper cells with the
level of expression of different cytokines networks and transcription factors.
Fourth, we did not evaluate the relative changes of frequencies of T-helper
subsets after treatment. Fifth, we did not evaluate the intracellular Foxp3
expression in Tregs.

In conclusion ,  in active pulmonary tuberculosis , T-helper
cells which is critical for anti-infection immunity are subjected to convert to
regulatory phenotypes  .Monitoring
PD1-PDL1 expression in LTBIs  and
manipulation PD1/PD-L1 pathway may help to 
evaluate and restore host protective immunity and prevent progression of
latent M.tb infection to active pulmonary tuberculosis. However the dynamic
changes of T-helper cells at the site of infection need further study to
correlation with changes that happen in peripheral blood and deserved further

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