Oligoclonal expansion of atypical Vδ2− γδ T cells in Good’s Syndrome
- Esther Bandala-Sanchez
- Laura Scolamiero
- Josh Chatelier
- Kerry A. Ramsay
- Alison Morey
- Sylvia Tsang
- Maureen Forde
- Julian J. Bosco
- Marsus Pumar
- Silvia Sanchez-Ramon
- Kissy Guevara-Hoyer
- Jesus Fuentes-Antras
- Jack Godsell
- Kymble Spriggs
- Anouk von Borstel
- Samantha Chan
- Lauren J. Howson
2026-06-11
Good’s syndrome is a rare adult-onset immunodeficiency 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 T cells, including γδ T cells, 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.