MAIT and Vδ2 unconventional T cells are supported by a diverse intestinal microbiome and correlate with favorable patient outcome after allogeneic HCT.

Journal Article (Journal Article)

Microbial diversity is associated with improved outcomes in recipients of allogeneic hematopoietic cell transplantation (allo-HCT), but the mechanism underlying this observation is unclear. In a cohort of 174 patients who underwent allo-HCT, we demonstrate that a diverse intestinal microbiome early after allo-HCT is associated with an increased number of innate-like mucosal-associated invariant T (MAIT) cells, which are in turn associated with improved overall survival and less acute graft-versus-host disease (aGVHD). Immune profiling of conventional and unconventional immune cell subsets revealed that the prevalence of Vδ2 cells, the major circulating subpopulation of γδ T cells, closely correlated with the frequency of MAIT cells and was associated with less aGVHD. Analysis of these populations using both single-cell transcriptomics and flow cytometry suggested a shift toward activated phenotypes and a gain of cytotoxic and effector functions after transplantation. A diverse intestinal microbiome with the capacity to produce activating ligands for MAIT and Vδ2 cells appeared to be necessary for the maintenance of these populations after allo-HCT. These data suggest an immunological link between intestinal microbial diversity, microbe-derived ligands, and maintenance of unconventional T cells.

Full Text

Duke Authors

Cited Authors

  • Andrlová, H; Miltiadous, O; Kousa, AI; Dai, A; DeWolf, S; Violante, S; Park, H-Y; Janaki-Raman, S; Gardner, R; El Daker, S; Slingerland, J; Giardina, P; Clurman, A; Gomes, ALC; Nguyen, C; da Silva, MB; Armijo, GK; Lee, N; Zappasodi, R; Chaligne, R; Masilionis, I; Fontana, E; Ponce, D; Cho, C; Bush, A; Hill, L; Chao, N; Sung, AD; Giralt, S; Vidal, EH; Hosszu, KK; Devlin, SM; Peled, JU; Cross, JR; Perales, M-A; Godfrey, DI; van den Brink, MRM; Markey, KA

Published Date

  • May 25, 2022

Published In

Volume / Issue

  • 14 / 646

Start / End Page

  • eabj2829 -

PubMed ID

  • 35613281

Pubmed Central ID

  • PMC9893439

Electronic International Standard Serial Number (EISSN)

  • 1946-6242

Digital Object Identifier (DOI)

  • 10.1126/scitranslmed.abj2829


  • eng

Conference Location

  • United States