Cytomegalovirus drives Vδ1+ γδ T cell expansion and clonality in common variable immunodeficiency

Samantha Chan, Benjamin Morgan, Michelle K. Yong, Mai Margetts, Anthony J. Farchione, Erin C. Lucas, Jack Godsell, Nhi Ai Giang, Charlotte A. Slade, Anouk Borstel, Vanessa L. Bryant and Lauren J. Howson ()
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Samantha Chan: Walter & Eliza Hall Institute of Medical Research
Benjamin Morgan: Walter & Eliza Hall Institute of Medical Research
Michelle K. Yong: Royal Melbourne Hospital
Mai Margetts: Walter & Eliza Hall Institute of Medical Research
Anthony J. Farchione: Walter & Eliza Hall Institute of Medical Research
Erin C. Lucas: Walter & Eliza Hall Institute of Medical Research
Jack Godsell: Royal Melbourne Hospital
Nhi Ai Giang: Royal Melbourne Hospital
Charlotte A. Slade: Walter & Eliza Hall Institute of Medical Research
Anouk Borstel: Monash University
Vanessa L. Bryant: Walter & Eliza Hall Institute of Medical Research
Lauren J. Howson: Walter & Eliza Hall Institute of Medical Research

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract The function and phenotype of γδ T cells in the context of common variable immunodeficiency (CVID) has not been explored. CVID is a primary immunodeficiency disorder characterized by impaired antibody responses resulting in increased susceptibility to infections. γδ T cells are a subset of unconventional T cells that play crucial roles in host defence against infections. In this study, we aim to determine the roles and functions of γδ T cells in CVID. We observe a higher frequency of Vδ1+ γδ T cells compared to healthy controls, particularly in older patients. We also find a higher proportion of effector-memory Vδ1+ γδ T cells and a more clonal T cell receptor (TCR) repertoire in CVID. The most significant driver of the Vδ1+ γδ T cell expansion and phenotype in CVID patients is persistent cytomegalovirus (CMV) viremia. These findings provide valuable insights into γδ T cell biology and their contribution to immune defence in CVID.

Date: 2024
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DOI: 10.1038/s41467-024-48527-3

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