Malaria has had an overwhelming impact on human lives and remains one of the most serious life-threatening infectious diseases in the world. Malaria is caused by infection with protozoan parasites from the genus Plasmodium and can present with a wide clinical spectrum. During Plasmodium infection there are multiple immune responses that are triggered to protect tissues and control parasite growth. These responses involve the activation of and interactions between many different immune cells. We recently discovered a molecule called NK cell granule protein 7 (NKG7) was an important mediator of inflammation in infectious diseases and cancer. NKG7 was first characterised in 1993 and has been shown to be expressed in different immune cell populations and implicated in both pro-inflammatory and anti-inflammatory responses. In many transcriptional studies, NKG7 was identified as a biomarker in various clinical and experimental contexts. However, its function in health and disease remains poorly characterised. This study reports on the role of NKG7 in CD4+ and CD8+ T cell responses during malaria. We identified key anti-parasitic roles for NKG7 in the generation and function of IFNγ+ Tbet+ T helper 1 (Th1) cells, IFNγ+ IL-10+ T regulatory 1 (Tr1) cells and CXCR5+ PD-1+ T follicular helper (Tfh) cells. Furthermore, we discovered a critical role for NKG7 in the generation of cytotoxic CD8+ T cells that mediate neurological damage in a pre-clinical model of cerebral malaria. Together, these findings provide a better understanding of the role of NKG7 in inflammation and support the therapeutic targeting of NKG7 for treatment of chronic infectious diseases.