Figure 6. Adaptive differentiation of human γδ T cells in vivo.

(A) Transition of Vγ9⁺Vδ1⁺ T cells to a T_effector transcriptional program following CMV infection after kidney transplantation involving increased Eomes⁺, HOBIT⁺, and granzyme B⁺ T_effector cells.

(B) Vγ9^negVδ2⁺ T cells transition from a predominantly CD27^hi, T-bet^neg, HOBIT^neg, BLIMP-1^neg phenotype to a CD27^lo/neg, T-bet⁺, HOBIT⁺, BLIMP-1⁺ phenotype 39 weeks post-CMV infection.

(C) Transition of Vδ1⁺ T cells from a T_naive to a T_effector transcriptional program following consecutive controlled human malaria challenge (CHMI) in two malarianaive individuals. (Left panel) Flow cytometry plots from one individual showing baseline (malaria naive), CHMI challenge 1 + 20 days after first infection and CHMI challenge 3 + 20 days and measure expression of T-bet, HOBIT, and Eomes versus CD27. (Right panel) Frequencies of T-bet⁺, HOBIT⁺, and Eomes⁺ Vδ1⁺ T cells from the same individual and second individual undergoing CHMI.

(D) Assessment of Vδ1⁺ T_effector (CD27^lo/neg) and CD8⁺ effector (T_CM + T_EM + T_EMRA) cells in 16 healthy children (aged 12 months to 12 years).

(E) Percentage of CD27^lo/neg Vδ1⁺ cells correlates with percentage of CD8⁺ effector αβ T cells (R² = 0.76, Spearman coefficient = 0.73, p = 0.0017).