PLZF, the signature transcription factor of innate T-lymphocytes, has been shown to confer elevated cell-surface expression of the integrin, LFA-1. While integrins are known to mediate both adhesive and signaling activities, the functional impact of LFA-1 expression by innate T lymphocytes remains poorly understood. Here we show that exposing human iNKT cells to high valencies of ICAM-1 (an adhesion ligand for LFA-1) is sufficient to induce their secretion of IFNγ in the absence of TCR or cytokine stimulation. iNKT cell IFNγ secretion via this LFA-1-mediated pathway required  mRNA transcription, and depended on calcium and MAPK signaling, but JAK-STAT activation was dispensible. Exposing primary human blood lymphocytes to high valency ICAM-1 revealed a responding T cell population that was highly enriched for PLZF⁺ cells, including iNKT cells, MAIT cells, and Vδ2⁺ T cells. Thus, this pathway of IFNγ production appears to be a shared feature of several human innate T-lymphocyte populations. These results indicate that innate T lymphocytes may contribute IFNγ in inflammatory contexts where ICAM-1 is upregulated e.g. multiple sclerosis, atherosclerosis and sepsis. Moreover, since this pathway is dependent on neither foreign antigens nor inflammatory cytokines, it may represent a mechanism for the production of "early" IFNγ that is thought to play a key role in defining the course of the subsequent response.