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Review
. 2023 Feb 17;24(4):4084.
doi: 10.3390/ijms24044084.

Graft-versus-Host Disease Modulation by Innate T Cells

Ying Fang  1 , Yichen Zhu  1 , Adam Kramer  1 , Yuning Chen  1 , Yan-Ruide Li  1 , Lili Yang  1   2   3   4
Affiliations
Review

Graft-versus-Host Disease Modulation by Innate T Cells

Ying Fang et al. Int J Mol Sci. .

Abstract

Allogeneic cell therapies, defined by genetically mismatched transplantation, have the potential to become a cost-effective solution for cell-based cancer immunotherapy. However, this type of therapy is often accompanied by the development of graft-versus-host disease (GvHD), induced by the mismatched major histocompatibility complex (MHC) between healthy donors and recipients, leading to severe complications and death VSports手机版. To address this issue and increase the potential for allogeneic cell therapies in clinical practice, minimizing GvHD is a crucial challenge. Innate T cells, encompassing subsets of T lymphocytes including mucosal-associated invariant T (MAIT) cells, invariant natural killer T (iNKT) cells, and gamma delta T (γδ T) cells, offer a promising solution. These cells express MHC-independent T-cell receptors (TCRs), allowing them to avoid MHC recognition and thus GvHD. This review examines the biology of these three innate T-cell populations, evaluates research on their roles in GvHD modulation and allogeneic stem cell transplantation (allo HSCT), and explores the potential futures for these therapies. .

Keywords: GvHD modulation; T-cell receptor (TCR); gamma delta T (γδ T) cell; graft-versus-host disease (GvHD); innate T cell; invariant natural killer T (iNKT) cell; major histocompatibility complex (MHC); mucosal-associated invariant T (MAIT) cell V体育安卓版. .

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VSports注册入口 - Conflict of interest statement

Y. -R. L. and L. Y. are inventors on patents relating to this article filed by UCLA. L. Y. is a scientific advisor to AlzChem and Amberstone Biosciences and a co-founder, stockholder, and advisory board member of Appia Bio V体育ios版. None of the declared companies contributed to or directed any of the research reported in this article. The remaining authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Targeting tumor and host cells by conventional αβ T (A), iNKT (B), MAIT (C), and γδ T cells (D). MHC–antigen–TCR interactions allow T cells to recognize target cells. MHC molecules on host cells could be recognized by conventional T cell TCRs after allogeneic cell infusion, resulting in GvHD. However, innate T cell TCRs do not recognize mismatched MHCs and protein antigens, therefore, these cells have no GVHD risk. MR1, major histocompatibility complex, class I-related protein; 5-OP-RU, 5-(2-oxopropylideneamino)-6-D-ribitylaminouracil.
Figure 2
Figure 2
GvHD modulation of innate T cells in cancer immunotherapy. (A) CAR-engineered innate T cells are generated from human peripheral blood mononuclear cells (PBMCs) or cord blood hematopoietic stem cells (HSCs). These CAR-engineered innate T cells could target cancers with high efficacy and low GvHD risk. (B) Allogeneic HSCs are engineered with innate T cell TCRs via lentiviral or retroviral transduction. Post-transplant reconstitution, innate T cells could be produced continuously to target cancers with reduced GvHD. (C) Donor innate T cells are expanded and coupled with HSCs for allogeneic HSC transplantation (HSCT). A low dose of innate T cells could potentially protect patients from GvHD. (D) Third-party innate T cells are generated from healthy donor PBMCs or cord blood HSCs and infused to cancer patients with allogeneic HSCs. Off-the-shelf innate T cells could provide a more convenient strategy for GvHD reduction.
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