Bandala Sánchez, EstherScolamiero, LauraChatelier, JoshRamsay, Kerry A.Morey, AlisonTsang, SylviaForde, MaureenBosco, Julian J.Pumar, MarsusGuevara Hoyer, Kissyet al.2026-08-042026-08-042026Bandala-Sanchez, E., Scolamiero, L., Chatelier, J., Ramsay, K. A., Morey, A., Tsang, S., Forde, M., Bosco, J. J., Pumar, M., Sanchez-Ramon, S., Guevara-Hoyer, K., Fuentes-Antrás, J., Godsell, J., Spriggs, K., Von Borstel, A., Chan, S., & Howson, L. J. (2026). Oligoclonal expansion of atypical Vδ2− γδ T cells in Good’s Syndrome. Nature Communications, 17(1), 7439. https://doi.org/10.1038/s41467-026-74273-92041-1723https://hdl.handle.net/11268/17357Good’ssyndromeisarareadult-onsetimmunodeficiency characterized by thymoma, hypogammaglobulinemia, B-cell lymphopenia, and T-cell dysfunction. Despite well-characterized defects in conventional immune subsets, the impact of this disorder on unconventional Tcells, including γδ Tcells, remains largely unexplored. In this study, we analyse γδ T cells in 10 patients with Good’s syndrome using immunophenotyping, functional assays, and T-cell receptor (TCR)δ repertoire profiling of peripheral blood and thymoma tissue. Our analyses reveal a pronounced expansion of the Vδ2⁻ γδ T-cell compartment, composed primarily of Vδ1⁺,Vδ3⁺ and the exceptionally rare Vδ8⁺ subsets. The Vδ2⁻ cells are characterized by an activated and effector phenotype and a private and oligoclonal TCRδ repertoire. The thymoma tissue contains distinct clonotypes compared to circulation, suggesting clonal focusing in response to the tumor. Together, our findings show that γδ T-cell perturbations are integral characteristics of Good’s syndrome and broaden our understanding of immune dysregulation in this acquired immunodeficiency.engAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/BiocienciasSíndromes de InmunodeficienciaTimomajournal article10.1038/s41467-026-74273-9open accessCiencias médicasInmunologíaCáncerGoal 3: Ensure healthy lives and promote well-being for all at all ages