SummaryTuberculous pleurisy is a naturally occurring site of Mycobacterium tuberculosis (Mtb) infection. Herein, we describe the expression of activation, natural killer (NK) and cell migration markers, as well as effector functions from gdT cells in peripheral blood (PB) and pleural effusion (PE) from tuberculosis patients (TB). We observed a decreased percentage of circulating gdT from TB patients and differential expression of NK as well as of chemokine receptors on PB and PE. Two subsets of gdT cells were differentiated by the CD3/gdT cell receptor (gdTCR) complex. The gdTCR low subset had a higher CD3 to TCR ratio and was enriched in Vd2 + cells, whereas most Vd1 + cells belonged to the gdTCR high subset. In PB from TB, most gdTCR high were CD45RA + CCR7 -and gdTCR low were CD45RA +/-CCR7 + CXCR3 + . In the pleural space the proportion of CD45RA -CCR7 + CXCR3 + cells was higher. Neither spontaneous nor Mtbinduced interferon (IFN)-g production was observed in PB-gdT cells from TB; however, PE-gdT cells showed a strong response. Both PB-and PE-gd T cells expressed surface CD107a upon stimulation with Mtb. Notably, PE-gdTCR low cells were the most potent effector cells. Thus, gdT cells from PB would acquire a further activated phenotype within the site of Mtb infection and exert full effector functions. As gdT cells produce IFN-g within the pleural space, they would be expected to play a beneficial role in tuberculous pleurisy by helping to maintain a T helper type 1 profile.