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The Special Issue on Immunobiology of Transplantation Mepur H www.symbiosisonline.org Symbiosis www.symbiosisonlinepublishing.com Opinion SOJ Immunology Open Access The Special Issue on Immunobiology of Transplantation Mepur H. Ravindranath* Terasaki Foundation Laboratory, 11570 W, Olympic Blvd, Los Angeles, California, USA Received: August 21, 2015; Accepted: October 02, 2015; Published: October 20, 2015 *Corresponding author: Mepur H. Ravindranath, Terasaki Foundation Laboratory, 11570 W, Olympic Blvd, Los Angeles, CA 90064, USA, Tel: +310-479-6101 ext. 103; Fax: +310-445-3381; E-mail: [email protected] The era of organ transplantation began when Emerich perspective. Five of them were conceived and written under Ullmann, an Austro-Hungarian professor of surgery, performed the leadership of Paul I. Terasaki, one of the pioneers in the development of organ transplanation, who is well known for the first intestinal transplant (1889), for which he was regarded transplantation. First, he developed the cytotoxicity assay to anastomosingas “the father aof pig intestinal kidney intotransplantation” the cubital region [1]. On of aMarch woman 7, matcha wide donorsarray of to contributions recipients [4], to exposing the field donor of immunobiology HLA-expressing of 1902, he performed the first kidney transplant on a human, monograph on the state of the art of transplantation, “Tissue molecules [5-7], and to prove their immunogenic capabilities with end-stage renal disease; the transplant failed. His 1914 [8,9]cells toin thevivo recipient’s. Third, after sera. recognizing Second, he thewas wide the first diversity to purify of HLA the insurmountable immunological barriers to transplantation alleles, he developed a reliable and reproducible methodology and Organ Transplantation”, summarized what then seemed immunosuppression were developed, becoming available in [1]. It would take almost 50 years before effective means of to monitor Donor-Specific HLA Antibodies (DSA); for this, he performed an autotransplant of a dog’s kidney to its throat. In Withused microbeadsthis technology, coated he withwas ablerecombinant to capture HLA critical molecules moments (both of the 1950s [2]. However, in 1902-Ullmann had successfully theHLA immune class -I rejectionand-II) analyzed of an allo-organ, by a Luminex which platformwas mediated [10,11]. by transplant of a dog’s kidney, showing that “such a transplant antibodies. As a result, Paul I Terasaki proposed the “Humoral doesn’t1908, French interfere surgeon with the Alexis kidney Carrel function,” performed which the meant same that, auto at least as a matter of surgery, organ transplantation was a reality. submitted by his team at the Terasaki Foundation Laboratory whichTheory highlightof Transplantation” a few aspects [12,13]. of This the issue immunobiology contains papers of transplantation. ofThis transplantation. earned Carrel the They Nobel included Prize in Sir 1912. Peter Subsequently, B. Medawar several, Sir F. In his manuscript, “The Model of Chronic Allograft Injury in Macfarlaneother Nobel Burnet, laureates Baruj laid Benacerraf, the foundation Jean for D.G.J. the Dausset,immunobiology George Alloantibody Positive Renal Transplant Patients”, Matthew J. Everly D. Snell, Joseph E. Murray and E. Donnall Thomas. summarizes the current concepts about chronic allograft injury Medawar postulated immunobiological forces inhibited the and allograft failure in transplant patients who are positive for DSA. survival of an allograft post-transplantation. The elucidation of He uses renal transplantation as a model, and highlights several inhibitory factors began with the discovery of transplantation important observations that build upon Terasaki’s Humoral theory of transplantation. Foremost, Everly indicates that the antigens on the cell surface of an allograft are recognized by clinical appearance of de novo DSA in many transplant patients theantigens, recipient’s called immune the “Human components Leukocyte as “non-self,”Antigens” (HLA).and immune These may be driven, primarily, by low immunosuppression states, attack commenced against the allograft. The reverse can also namely non-adherence to immunosuppression or physician- happen as in the case of bone marrow transplantation, where directed immunosuppression minimization. This report makes the immune cells of the allograft may recognize the recipient’s it clear that there is a need for a better understanding of DSA in cells as foreign and attack them, a phenomenon known as “Graft- have apparently normal intermediate-term allograft function, strategies to overcome organ, tissue or bone marrow rejection Everlytransplantation. suggests thatBy findingeither immunosuppression that 75% of DSA-positive currently patients in use Versus-Host Disease”(GvHD). Murray and Thomas suggested is working to suppress immunological injury or that there needs thatpost-transplantation goal is a holistic [3]. perspective But we are yetfollowed to succeed by a in reductionist making the Moving forward, Everly suggests that “completely” studying approachallo-organ to accepted the immunobiology as “self”. The of transplantation.first step necessary to reach theto be alloimmune a clarification response on the andinteraction the longitudinal of DSA with development the allograft. of allograft injury may be the next necessary step toward better The articles presented in this special issue aim at that dual Symbiosis Group *Corresponding author email: [email protected] The Special Issue on Immunobiology of Transplantation Copyright: © 2015 Ravindranath placed in the new microenvironment of the recipient. stratification of injury types undergone by the allograft after it is transplantation,the literature that, functioning the HLA-Ib as ligandsmolecules for (HLA-E,immunomodulatory HLA-F and cell-surfaceHLA-G) have inhibitory been emerging and activatingas potential receptors immune expressedregulators byof Junchao Cai, with Everly, Cheng, Terasaki, et al., uses the UNOS registry to compare allograft survival in ABO-compatible rejection. Jucaud, et al, underscores that this interaction is the subsets of NK and CD8+ T cells-the major players in allograft intestinal transplants performed in the US, with that of ABO- dependent on the nature and source of peptides presented. When HLA-Ia-derived peptides are presented by HLA-E, then donors,identical and transplants. blood group The AB ABO-compatible patients who received recipients transplants included blood group A and B patients who received allografts from O the HLA-E molecule interacts with inhibitory receptors to block the cytotoxic cell functions-thereby promoting graft survival. recipients experienced a significantly higher rate of acute re- from A, B, or O donors. ABO-compatible intestinal transplant- or viral or bacterial peptides, HLA-E interacts with activating receptorsHowever, towhen activate presenting the cytotoxic with cells,the leadingHLA-G toleader graft rejection.sequence maintenancejection than didimmunosuppressive ABO-identical patients, therapies. possibly Even due more to subim- portantjecting the than ABO-compatible the need for increased transplants immunosuppression, to intense induction/ the - familiesThe authors of receptors. show how In contrast,other HLA-Ib the overexpression molecules (HLA-G of HLA-Ib and cipients had a significantly higher rate of acute rejection, with HLA-F) may promote graft acceptance by binding to different Cai group found that ABO-compatible intestinal transplant re may promote GvHD in non-HLA-Ib-matched patients undergoing cell transplantation. Indeed, HLA-Ib molecules can become “non- group. The authors attribute that acute rejection to GvH anti- self” antigenic targets recognized by the donors’ cells when a >40% higher graft loss than recipients in the ABO-identical bodies that can be produced by viable graft-derived lympho- donors and recipients are not HLA-Ib identical. The occurrence kidney transplantation, GvH antibodies have been shown to in a soluble HLA-Ib state promotes greater immune modulation cytes from lymphoid tissues of allografts. In ABO-compatible andof HLA-Ib recognition. with or HLA-Ib without exposes β2-microglobulin epitopes to different(β2m) and immune being that the GvH reactions may damage host lymphoid tissues and cause hemolysis 60% of the time. The Cai group also points out produce profound immunosuppression leading to infection. and polyreactive antibodies with different functions, mediated by signalcomponents, transduction. contributing to the production of both monospecific on immune tolerance mechanisms observed in liver allograft Ravindranath, with Terasaki and Jucaud, review the Elaine Y. Cheng, with Terasaki, reviewed the literature recipients. The liver allograft has a lower incidence of rejection literature about the immunobiology of HLA in the allograft than do other solid organ transplants. The spontaneous microenvironment. We restrict our review to HLA-Ia and HLA-II, acceptance of the liver allograft after discontinuation of reporting that HLA molecules can promote allograft escape from on how current research has advanced our hopes of achieving pressure to an allograft. The physicochemical structure of immunosuppression (in 20% of allograft recipients) sheds light transplantation tolerance. The authors elaborate in detail the HLA-Icytotoxic and killing HLA-II and are elucidatedalso provide to understandcellular/ humoral their functional immune putative immune mechanisms underlying graft acceptance. potential. The importance of glycosylation of HLA molecules is These include sheltering
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