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Graft-versus-leukemia effect via alloreactive donor T cells (GVL effect)

Target: GVL effect
Molecular classification: Other (immunological process; involves various molecules such as T cell receptors, HLA molecules, and minor histocompatibility antigens but is not a single molecule)

Overview

The *graft-versus-leukemia (GVL) effect* is an immunological phenomenon observed after allogeneic hematopoietic cell transplantation, in which **alloreactive donor T cells recognize and eliminate recipient leukemia cells**, thereby reducing relapse risk and contributing to cure. This effect is mediated mainly by T lymphocytes recognizing peptides (from minor histocompatibility antigens, leukemia-associated antigens, or neoantigens) presented by HLA molecules on leukemia cells. The therapeutic goal is to maximize the GVL effect to prevent relapse, while minimizing graft-versus-host disease (GVHD), which results from similar alloreactive T cell responses against healthy recipient tissues.

Other names: Graft versus leukemia effectGvLGVL

Mechanism of action

Enhancement or suppression of donor T cell activation and function; Promotion of antigen presentation (via HLA/MHC); Modulation of T cell exhaustion or checkpoint molecule expression; Induction of apoptosis in leukemia cells via cytotoxic T lymphocyte (CTL) activity

Biological functions

Immune responseApoptosis (induced cell death of leukemia cells)Cancer immunityAlloimmunity

Disease associations

Cancer (specifically leukemia)

Safety considerations

Graft-versus-host disease (GVHD): immune attack on recipient healthy tissues by donor T cells, a major limitation of GVL effectImmune escape by leukemia cells (e.g., downregulation of HLA, exhaustion of T cells)Infection risk due to immune suppressionRelapse risk if GVL effect is inadequate

Interacting drugs

Donor lymphocyte infusions (DLI)

3 more in the full profile.

Biomarkers

Chimerism status (proportion of donor vs recipient cells)Expression of MHC/HLA molecules on leukemia cellsMinor histocompatibility antigens (miHA) and leukemia-associated antigensT cell receptor clonalityImmune checkpoint expression (such as PD-1)

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