Editing Transplant rejection (section)

==Rejection treatment==
{{More citations needed section|date=June 2020}}
Hyperacute rejection manifests severely and within minutes, and so treatment is immediate: removal of the tissue. Acute rejection is treated with one or several of a few strategies. Despite treatment, rejection remains a major cause of transplant failure.<ref>{{cite journal |display-authors=6 |vauthors=Naesens M, Kuypers DR, De Vusser K, Evenepoel P, Claes K, Bammens B, Meijers B, Sprangers B, Pirenne J, Monbaliu D, Jochmans I, Lerut E |date=August 2014 |title=The histology of kidney transplant failure: a long-term follow-up study |journal=Transplantation |volume=98 |issue=4 |pages=427–435 |doi=10.1097/TP.0000000000000183 |pmid=25243513 |s2cid=20703626|doi-access=free }}</ref> Chronic rejection is generally considered irreversible and poorly amenable to treatment—only retransplant generally indicated if feasible—though inhaled [[ciclosporin]] is being investigated to delay or prevent chronic rejection of lung transplants.

===Immunosuppressive therapy===

A short course of high-dose [[corticosteroids]] can be applied, and repeated. ''Triple therapy'' adds a [[calcineurin inhibitor]] and an [[anti-proliferative agent]]. Where calcineurin inhibitors or steroids are contraindicated, [[mTOR|mTOR inhibitors]] are used.

'''Immunosuppressive drugs''':
* [[Corticosteroids]]
** [[Prednisolone]]
** [[Hydrocortisone]]
* [[Calcineurin]] inhibitors
** [[Ciclosporin]]
** [[Tacrolimus]]
* Anti-proliferatives
** [[Azathioprine]]
** [[Mycophenolic acid]]
* [[mTOR]] inhibitors
** [[Sirolimus]]
** [[Everolimus]]

===Antibody-based treatments===

Antibody specific to select immune components can be added to immunosuppressive therapy. The [[monoclonal antibody|monoclonal]] anti-T cell antibody [[OKT3]], once used to prevent rejection, and still occasionally used to treat severe acute rejection, has fallen into disfavor, as it commonly brings severe [[cytokine release syndrome]] and late [[post-transplant lymphoproliferative disorder]]. (OKT3 is available in the [[United Kingdom]] for named-patient use only.)

'''Antibody drugs''':
* Monoclonal anti-IL-2Rα receptor antibodies
** [[Basiliximab]]
** [[Daclizumab]]
* Monoclonal anti-IL-6R receptor antibodies
** [[Tocilizumab]]
* Polyclonal anti-T-cell antibodies
** [[Anti-thymocyte globulin]] (ATG)
** [[Anti-lymphocyte globulin]] (ALG)
* Monoclonal anti-CD20 antibodies
** [[Rituximab]]

===Blood transfer===

Cases refractory to immunosuppressive or antibody therapy are sometimes treated with photopheresis, or extracorporeal photoimmune therapy (ECP), to remove antibody molecules specific to the transplanted tissue.

===Marrow transplant===

[[Bone marrow transplant]] can replace the transplant recipient's immune system with the donor's, and the recipient accepts the new organ without rejection. The marrow's [[hematopoietic stem cells]]—the reservoir of [[stem cells]] replenishing exhausted blood cells including [[white blood cells]] forming the immune system—must be of the individual who donated the organ or of an [[identical twin]] or a [[cloning|clone]]. There is a risk of [[graft-versus-host disease]] (GVHD), however, whereby mature [[lymphocytes]] entering with marrow recognize the new host tissues as foreign and destroy them.

===Gene therapy===
[[Gene therapy]] is another method that can be used. In this method, the genes that cause the body to reject transplants would be deactivated. Research is still being conducted, and no gene therapies are being used to date to treat patients.<ref>{{cite journal | vauthors = Yang JY, Sarwal MM | title = Transplant genetics and genomics | journal = Nature Reviews. Genetics | volume = 18 | issue = 5 | pages = 309–326 | date = May 2017 | pmid = 28286337 | doi = 10.1038/nrg.2017.12 | s2cid = 2222755 }}</ref><ref>{{cite journal | vauthors = Bagley J, Iacomini J | title = Gene therapy progress and prospects: gene therapy in organ transplantation | journal = Gene Therapy | volume = 10 | issue = 8 | pages = 605–611 | date = April 2003 | pmid = 12692588 | doi = 10.1038/sj.gt.3302020 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Giannoukakis N, Thomson A, Robbins P | title = Gene therapy in transplantation | journal = Gene Therapy | volume = 6 | issue = 9 | pages = 1499–1511 | date = September 1999 | pmid = 10490759 | doi = 10.1038/sj.gt.3300981 | doi-access = free }}</ref> Current research tends to focus{{fact|date=January 2022}} on Th1 and Th17 which mediate allograft rejection via the [[Cyclophosphamide#Mechanism of action|CD4]] and CD8 [[T-cell receptor|T cells]].<ref>{{cite journal | vauthors = Yuan X, Paez-Cortez J, Schmitt-Knosalla I, D'Addio F, Mfarrej B, Donnarumma M, Habicht A, Clarkson MR, Iacomini J, Glimcher LH, Sayegh MH, Ansari MJ | display-authors = 6 | title = A novel role of CD4 Th17 cells in mediating cardiac allograft rejection and vasculopathy | journal = The Journal of Experimental Medicine | volume = 205 | issue = 13 | pages = 3133–3144 | date = December 2008 | pmid = 19047438 | pmc = 2605226 | doi = 10.1084/jem.20081937 }}</ref>