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However, the relative effects of IL-21 on individual STAT proteins during the differentiation of T follicular helper (Tfh) cells and GC B cells has been difficult to distinguish. Here, we characterize a novel mutation in the interleukin-21 receptor (IL-21R\n                    <jats:sup>EINS<\/jats:sup>\n                    ) that creates a dominant defect in the activation of STAT1. Our findings provide evidence that IL-21-mediated activation of STAT1 has a non-redundant role in the differentiation of Tfh cells following T-dependent immunization. IL-21R\n                    <jats:sup>EINS<\/jats:sup>\n                    Tfh cells were even more impaired than Tfh cells genetically deficient in IL-21R, questioning our current understanding of the role of IL-21 derived from protein knockout mice. The observation that functional compensation fails in the presence of the IL-21R hypomorph provides insight into how underlying compensation can impact our interpretation of a complex biological system.\n                  <\/jats:p>","DOI":"10.7554\/elife.109834","type":"journal-article","created":{"date-parts":[[2026,2,6]],"date-time":"2026-02-06T16:30:16Z","timestamp":1770395416000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.109834","source":"Crossref","is-referenced-by-count":0,"title":["An IL-21R STAT hypomorph circumvents functional redundancy in germinal centre responses"],"prefix":"10.7554","volume":"15","author":[{"given":"Christoph","family":"Jandl","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/01b3dvp57","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Immunology, Garvan Institute of Medical Research","place":["Darlinghurst, 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