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Ni L et aldemonstrated high levels of PD-1 expressions on Tregsin in the peripheral blood of subjects with hepatitis C virus lymphoma ( HCV-L) compared to non-HCV-L and blockingof PD1-PDL1 pathway  reduced the numberof Tregs and suppressed T-cell activation and proliferation in HCV-L waspartially restored.14   We also found that   expressionof PD1 on CD4+  T-cells and its ligands(PD-L1)in monocytes  were much higher in APTBspatients , which was in accordance with results of study done by Shen Let al.

4 Increased expressionof 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   Collectively our findings   apparently   indicate that,  a dynamic imbalance between proportionof  T-cell subpopulations  follow in M.tb infection and  conversion  of T-helper cells  to negative sub-populations severely impairedcell mediated immunity and contributed to development of active tuberculosisand PD1-PDL1  has a role in conversionand maintenance of Treg in active pulmonary tuberculosis .     There are several limitatons to the present study. First, the number ofcases was small.

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Second during the selection of latently infected individuals,we did not consider the nutritional level of study subjects which may influencethe IGRA and montoux test and may give false negative results. Third, we didnot correlate the changes in functional phenotypes of T-helper cells with thelevel of expression of different cytokines networks and transcription factors.Fourth, we did not evaluate the relative changes of frequencies of T-helpersubsets after treatment. Fifth, we did not evaluate the intracellular Foxp3expression in Tregs.In conclusion ,  in active pulmonary tuberculosis , T-helpercells which is critical for anti-infection immunity are subjected to convert toregulatory phenotypes  .

MonitoringPD1-PDL1 expression in LTBIs  andmanipulation PD1/PD-L1 pathway may help to evaluate and restore host protective immunity and prevent progression oflatent M.tb infection to active pulmonary tuberculosis. However the dynamicchanges of T-helper cells at the site of infection need further study tocorrelation with changes that happen in peripheral blood and deserved furtherstudy.

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