The present invention relates to methods for modulating innate lymphoid cell activity, antibody drug conjugates and uses in therapy. The inventors showed in a model of murine cytomegalovirus infection, that glucocorticoid receptor expression in innate lymphoid cells plays an essential early role in regulating host protection against inflammation-induced tissue damage. Mechanistically, they demonstrated for the first time that endogenous glucocorticoids produced shortly after infection promote the expression of the immune checkpoint PD1 on the surface of natural killer cells. This glucocorticoid-PD1 pathway acts to limit the production of interferon-γ by NK cells. The modulation of the glucocorticoid-PD1 pathway in order to increase or decrease the activity of ILCs would permit to treat either cancers and infectious diseases or autoimmune and inflammatory diseases. In particular, the present invention relates to a method of modulating innate lymphoid cell activity which comprises modulating the activity of glucocorticoid receptor.