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More recently, immunotherapy has emerged to restore immunity against infectious agents, including bacterial infections. Immunotherapy primarily targets inhibitory pathways in T cells, however interest in other effector populations, such as natural killer (NK) cells, is growing. We have previously discovered that NK cell metabolism, proliferation and activation can be neutralized through the immunosuppressive transforming growth factor (TGF)\u2010\u03b2 pathway by inducing plasticity of NK cells and differentiation into innate lymphoid cell (ILC)1\u2010like subsets. NK cells are also regulated through cytokine\u2010inducible SH2\u2010containing protein (CIS), which is induced by interleukin (IL)\u201015 and is a potent intracellular checkpoint suppressing NK cell survival and function. Targeting these two distinct pathways to restore NK cell function has shown promise in cancer models, but their application in bacterial infection remains unknown. Here, we investigate whether enhancement of NK cell function can improve anti\u2010bacterial immunity, using <jats:italic>Salmonella<\/jats:italic> Typhimurium as a model. We identified conversion of NK cells to ILC1\u2010like for the first time in the context of bacterial infection, where TGF\u2010\u03b2 signalling contributed to this plasticity. Future study should focus on identifying further drivers of ILC1 plasticity and its functional implication in bacterial infection model. We further describe that CIS\u2010deficient mice displayed enhanced pro\u2010inflammatory function and dramatically enhanced anti\u2010bacterial immunity. Inhibition of CIS may present as a viable therapeutic option to enhance immunity towards bacterial infection.<\/jats:p>","DOI":"10.1111\/imm.13516","type":"journal-article","created":{"date-parts":[[2022,5,25]],"date-time":"2022-05-25T07:23:30Z","timestamp":1653463410000},"page":"54-63","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["<scp>CIS<\/scp> and <scp>TGF<\/scp>\u2010\u03b2 regulatory pathways influence immunity to bacterial infection"],"prefix":"10.1111","volume":"167","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0247-7374","authenticated-orcid":false,"given":"Timothy R.","family":"McCulloch","sequence":"first","affiliation":[{"name":"University of Queensland Diamantina Institute, Faculty of Medicine The University of Queensland  Woolloongabba QLD Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gustavo R.","family":"Rossi","sequence":"additional","affiliation":[{"name":"University of Queensland Diamantina Institute, Faculty of Medicine The University of Queensland  Woolloongabba QLD Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaring","family":"Schreuder","sequence":"additional","affiliation":[{"name":"University of Queensland Diamantina Institute, Faculty of Medicine The University of Queensland  Woolloongabba QLD Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabrielle T.","family":"Belz","sequence":"additional","affiliation":[{"name":"University of Queensland Diamantina Institute, Faculty of Medicine The University of Queensland  Woolloongabba QLD Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Timothy J.","family":"Wells","sequence":"additional","affiliation":[{"name":"University of Queensland Diamantina Institute, Faculty of Medicine The University of Queensland  Woolloongabba QLD 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