Graft-versus-host disease causes

Graft-versus-host disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]

## Overview[edit | edit source]

The major cause of GvHD is HLA disparity between the recipient and host, resulting in abnormal immune activation against the recipient. This concept was proposed by Billingham in the 1960s.

## Causes[edit | edit source]

According to the Billingham Criteria, 3 criteria must be met in order for GvHD to occur.[1]

* Administration of an immunocompetent graft, with viable and functional immune cells.
* The recipient is immunologically disperate and histoincompatible.
* The recipient is immunocompromised and therefore cannot destroy or inactivate the transplanted cells.

After bone marrow transplantation, T cells present in the graft, either as contaminants or intentionally introduced into the host, attack the tissues of the transplant recipient after perceiving host tissues as antigenically foreign. The T cells produce an excess of cytokines, including TNF alpha and interferon-gamma (IFNg). A wide range of host antigens can initiate graft-versus-host-disease, among them the human leukocyte antigens (HLAs). However, graft-versus-host disease can occur even when HLA-identical siblings are the donors. HLA-identical siblings or HLA-identical unrelated donors often have genetically different proteins (called minor histocompatibility antigens) that can be presented by MHC molecules to the recipient's T cells, which see these antigens as foreign and so mount an immune response.

While donor T cells are undesirable as effector cells of GvHD, they are valuable for engraftment by preventing the recipient's residual immune system from rejecting the bone marrow graft (host-versus-graft). Additionally, as bone marrow transplantation is frequently used to treat cancer, mainly leukemias, donor T cells have proven to have a valuable graft-versus-tumor effect. A great deal of current research on allogeneic bone marrow transplantation involves attempts to separate the undesirable graft-vs-host-disease aspects of T cell physiology from the desirable graft-versus-tumor effect.

## References[edit | edit source]

1. ↑ Villa NY, Rahman MM, McFadden G, Cogle CR (2016). "Therapeutics for Graft-versus-Host Disease: From Conventional Therapies to Novel Virotherapeutic Strategies". Viruses. 8 (3): 85. doi:10.3390/v8030085. PMC 4810275. PMID 27011200.CS1 maint: Multiple names: authors list (link)

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