Graft-versus-host disease causes: Difference between revisions
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*The recipient is immunocompromised and therefore cannot destroy or inactivate the transplanted cells. | *The recipient is immunocompromised and therefore cannot destroy or inactivate the transplanted cells. | ||
After bone marrow transplantation, [[T cell]]s present in the [[medical grafting|graft]], either as contaminants or intentionally introduced into the host, attack the [[biological tissue|tissues]] of the transplant recipient after perceiving host tissues as antigenically foreign. The T cells produce an excess of [[cytokine]]s, 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 [[Human leukocyte antigen|HLA]]-identical siblings are the donors. HLA-identical siblings or HLA-identical unrelated donors often have genetically different [[protein]]s (called minor histocompatibility antigens) that can be presented by [[Major histocompatibility complex|MHC]] molecules to the recipient's T | After bone marrow transplantation, [[T cell]]s present in the [[medical grafting|graft]], either as contaminants or intentionally introduced into the host, attack the [[biological tissue|tissues]] of the transplant recipient after perceiving host tissues as antigenically foreign. The [[T cells]] produce an excess of [[cytokine]]s, 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 [[Human leukocyte antigen|HLA]]-identical siblings are the donors. [[HLA]]-identical siblings or HLA-identical unrelated donors often have genetically different [[protein]]s (called minor histocompatibility antigens) that can be presented by [[Major histocompatibility complex|MHC]] molecules to the recipient's T cells, which see these antigens as foreign and so mount an immune response. | ||
While donor [[T | While donor [[T cell]]s 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 [[leukemia]]s, 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== | ==References== | ||
Revision as of 21:31, 21 June 2017
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Graft-versus-host disease |
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Differentiating Graft-versus-host disease from other Diseases |
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Graft-versus-host disease causes On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]
Overview
The major cause of GvHD is HLA disparity between the recipient and host, resulting in abnormal immune activation against the recipient.
Causes
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
- ↑ 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.