Although central roles of T helper 2 (Th2) cells, group 2 innate lymphoid cells (ILC2s) and IgE-producing B cells in allergic diseases are unquestionable, there is a growing body of evidence for regulation of allergic inflammation by other lymphocytes, including natural killer (NK) cells. In normal non-allergic humans and mice, NK cells produce IFNγ and exhibit cytotoxicity. As such, during a viral respiratory infection of normal mice, NK cells block the type-2 immune response, and prevent immune and stromal cell rewiring for allergic disease. Under influence of air pollutants, allergens, and the allergic inflammatory milieu, NK cells modify their molecular program, reduce IFNγ synthesis, begin to produce type-2 cytokines, and start to secrete granzyme B into the extracellular space, leading to activation of protease-activated receptors (PARs) on nearby cells. These new NK cell functions result in the enhancement of the type-2 immune response and allergic disease. This chapter summarizes current knowledge on the reciprocal relationship between NK cells and allergic inflammation in humans and mice. We also discuss how environmental exposures shape this relationship.