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The IL-2 receptor (IL-2R) is composed of IL-2R\u03b1, IL-2R\u03b2, and IL-2R\u03b3 subunits, with defects in IL-2R\u03b1 and IL-2R\u03b3 and their downstream signaling effectors resulting in known primary immunodeficiency disorders. Here, we report the first human defect in IL-2R\u03b2, occurring in two infant siblings with a homozygous IL2RB mutation in the WSXWS motif, manifesting as multisystem autoimmunity and susceptibility to CMV infection. The hypomorphic mutation results in diminished IL-2R\u03b2 surface expression and dysregulated IL-2\/15 signaling, with an anticipated reduction in regulatory T cells. However, in contrast to the IL-2R\u03b2\u2212\/\u2212 animal model, which lacks NK cells, these siblings demonstrate an expansion of NK cells, particularly the CD56bright subset, and a lack of terminally differentiated NK cells. Thus, the early-onset autoimmunity and immunodeficiency are linked to functional deficits arising from altered IL-2R\u03b2 expression and signaling in T and NK cells.<\/jats:p>","DOI":"10.1084\/jem.20182015","type":"journal-article","created":{"date-parts":[[2019,4,30]],"date-time":"2019-04-30T18:46:12Z","timestamp":1556649972000},"page":"1255-1267","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":90,"title":["A novel human <i>IL2RB<\/i> mutation results in T and NK cell\u2013driven immune dysregulation"],"prefix":"10.1084","volume":"216","author":[{"given":"Isabel Z.","family":"Fernandez","sequence":"first","affiliation":[{"name":"Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryan M.","family":"Baxter","sequence":"additional","affiliation":[{"name":"Department of Immunology and Microbiology, University of 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