Long-term low-dose dietary rapamycin specifically reduced IL-17-producing gamma delta T cells in aging mice without broadly suppressing immune function. The treatment particularly targeted these inflammatory cells in the peritoneal cavity and correlated with reduced circulating IL-17 levels and attenuated microglial inflammation following immune challenge. Importantly, other immune cell populations remained largely unchanged. This finding addresses a critical concern about rapamycin as a longevity intervention. While rapamycin is known as a potent immunosuppressant in clinical transplant doses, this research suggests that chronic low-dose exposure may achieve anti-aging benefits through selective immune modulation rather than wholesale suppression. The specific targeting of gamma delta T cells is particularly intriguing, as these cells are key drivers of inflammaging—the chronic low-grade inflammation that accelerates aging processes. The preservation of overall immune architecture while dampening harmful inflammatory pathways represents an ideal therapeutic profile for aging interventions. However, this remains mouse research requiring human validation, and the long-term consequences of selectively suppressing these T cell populations in humans remains unknown. The work provides mechanistic insight into how rapamycin might extend healthspan without compromising immune defense.