Negative regulation of innate lymphoid cell responses in inflammation and cancer

The immune system employs an array of effector cells to ensure tissue homeostasis and protection against pathogens. Lymphocytes belonging to both the adaptive and innate branches share several functions, comprising the ability to directly kill stressed or transformed cells, and to provide helper responses through specific production of cytokines. These properties are regulated by distinct sets of soluble molecules, receptors, and intracellular factors, which altogether tune the functional output of effector lymphocytes and their final activation state. In contrast to adaptive T cells, innate lymphoid cells (ILCs) do not require antigen receptors and are characterized for their ability to provide rapid immune responses. While the factors underlying functional diversification and the main principles leading to ILC activation have been dissected, our understanding of the mechanisms underlying termination of ILC effector functions is still in its infancy. Herein, we discuss the recent findings describing how ILC responses are turned off in the context of inflammation and cancer.