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Neutrophils play a key role in the innate immune system's response to infection. They eliminate microbes through phagocytosis, the production of ROS, and the secretion of various proteases and antimicrobial peptides. In addition, they influence adaptive immune responses by modulating B-cell antibody production, dendritic cell activation and anti-microbial CD4(+) and CD8(+) T-cell responses. Here we discuss the current knowledge of the reciprocal interactions between neutrophils and T cells. A special emphasis is put on their interaction with γδ T cells, which respond in the early stages of infection to produce a pivotal source of neutrophil-recruiting IL-17. Human peripheral blood γδ T cells are activated by microbe-derived and endogenous isoprenoid pyrophosphate antigens, the levels of which can be enhanced by the therapeutic application of aminobisphosphonates. We specifically discuss intriguing new evidence showing how pyrophosphates and aminobisphosphonates modulate the interplay between neutrophils and human γδ T cells.
Kalyan et al. (Fri,) studied this question.