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Vγ9/Vδ2⁺ T cells specifically recognize Mycobacterium tuberculosis in vitro and are precociously recruited in early mycobacterial lesions. Even if γ δ T cells are only fortuitously detected in granulomas or bronchoalveolar lavages of patients with active pulmonary tuberculosis, a role in shaping the mature α β T cell response against M. tuberculosis is substantiated. Here we provide a molecular explanation for this paradox: the engagement of the γ δ TCR by mycobacterial antigens induced the expression of CD95 ligand (CD95L) by chronically activated CD95⁺ /CD95L⁻ γ δ T lymphocytes. The receptor was functional, as CD95/CD95L interaction triggered the bystander death of CD95⁺ cells by apoptosis. Cell death was abolished by CD95-blocking antibodies. The transient accumulation at the site of infection of CD95L⁺ γ δ lymphocytes, capable of interacting with CD95⁺ leukocytes attracted by the response towards the pathogen, may determine the characteristics of the ensuing granulomatous disease.