Transmigration of γδ T cells in response to CXC or CC chemokines is inhibited by Tat, present in the serum of HIV-1 patients, because of the CXC or CC-like sequences. Vδ2 (A) or Vδ1 (B) cell lines from healthy donors were assayed for transmigration across HUVEC at 60 minutes, in the presence of 50 ng/mL IP-10/CXCL10 (A, □) or SDF-1/CXCL12 (B, □) or I-309/CCL1 (A-B, ▦), as described in “Patients, materials, and methods.” In some experiments, cells were exposed to 0.1 μg/mL Tat24-51 peptide wild type or mutated in the CXC (Tat25-27 Ala) or in the CC (30-31 Ala) sequence, as indicated. Nil indicates migration in the presence of the indicated chemokine, without Tat peptides. Results are expressed as percentage of cell migration, calculated as described in “Patients, materials, and methods” (mean ± SD from 4 independent experiments with cell lines from 4 donors). *Student t test; P < .05. (C-D) Vδ2 (C) or Vδ1 (D) T-cell lines obtained from 2 HIV-1–infected patients (patient 18, □; and patient 21, ▨) were assayed for transmigration across HUVEC monolayers at 60 minutes, in the presence of 50 ng/mL IP-10/CXCL10 (C) or SDF-1/CXCL12 (D), as described in “Patients, materials, and methods.” In some experiments, cells were preincubated with 0.1 μg/mL Tat or with autologous serum (1:2 dilution) alone or with an anti-Tat antiserum (1:400 dilution), as indicated. Nil indicates migration in the presence of the indicated chemokine, without Tat. Results are expressed as percentage of cell migration, calculated as described in “Patients, materials, and methods,” and are the mean ± SD from 3 independent experiments. *Student t test; P < .05.