The immune system has evolved to control and eliminate invading pathogens. Regulation of the immune responses generated during infection is essential to prevent immunopathology and autoimmunity. We have used murine cytomegalovirus (MCMV) infection as a model to investigate how the immune response to a pathogen capable of persisting within the host is regulated. While MCMV replication is rapidly controlled in most organs, viral replication persists long-term in salivary glands. In this tissue, the control of viral replication is mediated by CD4⁺ T cells. In addition to the recruitment of CD4⁺ T cells, group 1 innate lymphoid cells (ILCs) accumulate within salivary glands following MCMV infection. However, ILCs do not contribute to viral control, but rather limit anti-viral CD4⁺ T cell responses. While limiting anti-viral T cell responses results in prolonged chronic viral infection, the regulatory action of ILCs limits the generation of auto-reactive immune responses and resulting tissue damage. Using newly identified group 1 ILC phenotypic markers, we have characterised group 1 ILCs – comprised of Natural Killer (NK) cells and ILC1s – present in the salivary gland both in steady state and over the course of MCMV infection. We found that the cells involved in immune-regulation are a population of mature NK cells that are recruited into the salivary gland in response to infection, rather than a tissue-resident population of ILC1. Our data thereby identify a new population of NK cells critical for regulating immune responses to a common viral pathogen.