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    what happens at a cellular level during organ rejection

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    Transplant rejection: MedlinePlus Medical Encyclopedia

    Transplant rejection is a process in which a transplant recipient's immune system attacks the transplanted organ or tissue.

    Transplant rejection

    Transplant rejection is a process in which a transplant recipient's immune system attacks the transplanted organ or tissue.

    Causes

    Your body's immune system usually protects you from substances that may be harmful, such as germs, poisons, and sometimes, cancer cells.

    These harmful substances have proteins called antigens coating their surfaces. As soon as these antigens enter the body, the immune system recognizes that they are not from that person's body and that they are "foreign," and attacks them.

    When a person receives an organ from someone else during transplant surgery, that person's immune system may recognize that it is foreign. This is because the person's immune system detects that the antigens on the cells of the organ are different or not "matched." Mismatched organs, or organs that are not matched closely enough, can trigger a blood transfusion reaction or transplant rejection.

    To help prevent this reaction, doctors type, or match both the organ donor and the person who is receiving the organ. The more similar the antigens are between the donor and recipient, the less likely that the organ will be rejected.

    Tissue typing ensures that the organ or tissue is as similar as possible to the tissues of the recipient. The match is usually not perfect. No two people, except identical twins, have identical tissue antigens.

    Doctors use medicines to suppress the recipient's immune system. The goal is to prevent the immune system from attacking the newly transplanted organ when the organ is not closely matched. If these medicines are not used, the body will almost always launch an immune response and destroy the foreign tissue.

    There are some exceptions, though. Cornea transplants are rarely rejected because the cornea has no blood supply. Also, transplants from one identical twin to another are almost never rejected.

    There are three types of rejection:

    Hyperacute rejection occurs a few minutes after the transplant when the antigens are completely unmatched. The tissue must be removed right away so the recipient does not die. This type of rejection is seen when a recipient is given the wrong type of blood. For example, when a person is given type A blood when he or she is type B.

    Acute rejection may occur any time from the first week after the transplant to 3 months afterward. All recipients have some amount of acute rejection.

    Chronic rejection can take place over many years. The body's constant immune response against the new organ slowly damages the transplanted tissues or organ.

    Organ Transplantation

    NIH MedlinePlus Magazine

    Health Topics A-Z

    Source : medlineplus.gov

    Cellular Rejection

    Cellular Rejection

    Cellular rejection of transplanted tissue occurs, unless the donor and recipient are genetically identical or the host immune response has been suppressed.

    From: Little and Falace's Dental Management of the Medically Compromised Patient (Eighth Edition), 2013

    Related terms:

    Human Leukocyte AntigenSerositisBiopsyTransplantationAntibodyAllograftImmunosuppressive TreatmentAntibody Mediated RejectionAcute Graft RejectionChronic Graft Rejection

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    Liver and Hepatocyte Xenotransplantation∗

    Jeffrey L. Platt, ... Ira J. Fox, in Transplantation of the Liver (Third Edition), 2015

    Cellular Rejection

    Cellular rejection is potentially a more important hurdle to xenotransplantation of the liver because so many xenogeneic antigens are produced and secreted.69 Human T cells respond strongly to porcine cells, although that response can be more challenging to measure than allogeneic response.

    Besides conventional cellular immune responses, natural killer cells exhibit potent effector functions against xenogeneic targets. Natural and induced immunoglobulin G antibodies can amplify natural killer cell activity. Natural killer cells pose the greatest threat to cellular grafts, although recent work with allogeneic systems suggests they could also damage organ grafts.

    Macrophages can phagocytose porcine cells in an antibody- and complement-independent manner. Macrophages can be stimulated to phagocytosis by xenogeneic agonists and by failure of signal regulatory protein alpha, which interacts with CD47, to inhibit phagocytosis.

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    Heart Transplant

    In Diagnostic Pathology: Cardiovascular (Second Edition), 2018

    KEY FACTS

    Etiology/Pathogenesis

    Cellular rejection (CR)

    T-cell mediated host response to allografted heart stimulated by "foreign" human leukocyte antigen (HLA) and other antigens expressed in graft tissue

    Antibody-mediated rejection (AMR)

    Antibody-mediated host response to allografted heart with damage with complement activation

    Cardiac allograft vasculopathy (CAV)

    Arterial narrowing due to concentric intima thickening by proliferating smooth muscle cells and fibroblasts

    Clinical Issues

    Most rejection episodes occur within 6 months post transplant

    Macroscopic

    • Rejection ○

    May appear grossly normal

    • CAV ○

    Epicardial and intramyocardial artery involvement

    • Complications ○

    Malignancy (masses, lymphadenopathy)

    Infection (pneumonia, abscess, meningitis, pyelonephritis)

    Medication toxicity (cushingoid features, nephrosclerosis)

    Microscopic

    • CR ○

    Perivascular/interstitial mononuclear inflammation

    Myocyte damage in association with mononuclear inflammation

    • AMR ○

    Capillary endothelial cell swelling and injury

    Positive staining for complement (C4d and C3d)

    • CAV ○

    Marked concentric intima thickening

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    Pathology of Liver Transplantation

    Romil Saxena MD, FRCPath, M. Isabel Fiel MD, FAASLD, in Practical Hepatic Pathology: a Diagnostic Approach (Second Edition), 2018

    Late Cellular Rejection

    Late cellular rejection occurring 6 months after transplantation does not show the classical features of acute cellular rejection described previously; as the time after transplantation increases, the reaction seems to be “toned down” or “muted.” Endotheliitis and bile duct damage may be neither prominent nor extensive, and the portal inflammatory infiltrate may not contain many blastic lymphocytes or eosinophils (see eSlide 38.5) (Fig. 38.12). The presence of a chronic portal infiltrate without blastic lymphocytes, endotheliitis, and bile duct injury mimics chronic hepatitis and triggers serologic and other investigations to rule out various causes of chronic hepatitis; when these are negative, the biopsy may be labeled idiopathic chronic hepatitis (discussed in detail later) (Fig. 38.13).32

    A characteristic pattern of late graft injury consists of an intense plasma cell infiltrate in portal tracts with variable interface hepatitis (Fig. 38.14). The portal tract changes may be accompanied by central perivenulitis with a predominant plasma cell infiltrate. Alternatively, a plasma cell–rich perivenular infiltrate may be present without portal tract changes. This pattern of injury is variably referred to as de novo AIH or plasma cell hepatitis and is thought to represent late cellular rejection in at least some cases (discussed in detail later).

    Thus, late cellular rejection may show at least three atypical histologic variants, namely, idiopathic chronic hepatitis (ICP), and de novo–autoimmune–plasma cell hepatitis. However, each of these patterns (discussed in detail later) may also represent other posttransplant diseases in the allograft, which need to be distinguished from rejection to ensure appropriate management of immunosuppression.

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    Acute Cellular Rejection

    Madhav C. Menon, ... Fadi El Salem, in Kidney Transplantation, Bioengineering and Regeneration, 2017

    32.6.1 Treatment of Subclinical Rejection

    The treatment of SCR identified incidentally on biopsy has proven more controversial. While some randomized studies have suggested that treatment of SCR in early biopsies (1, 3, or 6 months) is associated with improvements in later renal function (1 or 2 years),18,95 a large randomized trial in the tacrolimus era showed a significantly lower prevalence of SCR and did not identify a benefit at 2 years by treating these SCR episodes.15 The treatment strategy for borderline changes seen on allograft biopsies is also without consensus. Most centers, including ours, treat these episodes with short courses of oral steroids, especially if associated with renal dysfunction. Transcriptional data from some studies have suggested that borderline changes may be a part of a continuum between ACR and non-ACR,81 while other groups have identified that borderline changes can be grouped clearly into either ACR or non-ACR.131 Intriguingly, studies have suggested increased regulatory T-cell activity in blood or allograft of biopsies with borderline ACR, when compared to both ACR and non-ACR.132,133 The presence of ABMR along with ACR (i.e., mixed rejection) requires aggressive treatment, is associated with less complete response to therapy, and is discussed in Chapter 35.

    Source : www.sciencedirect.com

    Mechanism of cellular rejection in transplantation

    The explosion of new discoveries in the field of immunology has provided new insights into mechanisms that promote an immune response directed against a transplanted organ. Central to the allograft response are T lymphocytes. This review summarizes the ...

    Pediatr Nephrol. 2010; 25(1): 61–74.

    Published online 2010 Jan 1. doi: 10.1007/s00467-008-1020-x

    PMCID: PMC2778785 PMID: 21476231

    Mechanism of cellular rejection in transplantation

    Elizabeth Ingulli1,2

    Author information Article notes Copyright and License information Disclaimer

    This article has been cited by other articles in PMC.

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    Abstract

    The explosion of new discoveries in the field of immunology has provided new insights into mechanisms that promote an immune response directed against a transplanted organ. Central to the allograft response are T lymphocytes. This review summarizes the current literature on allorecognition, costimulation, memory T cells, T cell migration, and their role in both acute and chronic graft destruction. An in depth understanding of the cellular mechanisms that result in both acute and chronic allograft rejection will provide new strategies and targeted therapeutics capable of inducing long-lasting, allograft-specific tolerance.

    Keywords: Allograft, Children, Rejection, T lymphocytes, TransplantationLearning objectives:

    To review recent advances in understanding the mechanisms of allograft rejection

    To outline the current data on allorecognition and its role in allograft rejection

    To discuss current therapeutics targeting costimulatory pathways

    To briefly discuss recent data on the role T regulatory and memory T cells play in alloimmune responses

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    Introduction

    Transplantation of solid organs has emerged as a viable therapeutic modality for the treatment of a variety of ailments, such as end stage renal disease. Acute allograft rejection is understood as an impediment to long-term allograft survival, increasing the risk of developing chronic rejection and decreasing allograft half-life by 34% [1]. With the widespread use of potent immunosuppressive drugs, early graft loss due to acute rejection has decreased dramatically; however, current immunosuppressive protocols have not reduced the rates of graft loss due to chronic rejection and have increased the risk of serious complications, such as life-threatening infections and cancers [2].

    Rejection of solid organ allografts is the result of a complex series of interactions involving coordination between both the innate and adaptive immune system with T cells central to this process. The ability of recipient T cells to recognize donor-derived antigens, called allorecognition, initiates allograft rejection. Once recipient T cells become activated, they undergo clonal expansion, differentiate into effector cells, and migrate into the graft where they promote tissue destruction. In addition, CD4 T cells help B cells produce alloantibodies. Here, we will review the components of an anti-allograft adaptive immune response.

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    Allorecognition

    Antigens that activate the immune system against the allograft, i.e. alloantigens, are both major and minor histocompatibility antigens. The major histocompatibility complex (MHC), located on chromosome 6 in humans, encodes the human leukocyte antigens (HLA), which are polymorphic molecules responsible for eliciting the strongest of responses to allogeneic tissues. The genes in this region encode for class I (HLA-A, -B, -C) and class II (HLA-DR, -DP, -DQ) molecules. The function of MHC molecules is to present foreign antigens to T cells. It has been known for more than 30 years that the T cell receptor (TCR) present on the surface of the T cell interacts with a peptide bound in the groove of the MHC molecule present on the surface of the antigen presenting cell. CD8 T cells recognize peptide/MHC class I complexes. MHC class I molecules are constitutively expressed on the surface of virtually all nucleated cells. CD4 T cells recognize peptide/MHC class II complexes. MHC class II molecules are constitutively expressed on the surface of professional antigen presenting cells, but expression can be induced on many cell types with activation.

    Minor histocompatibility antigens are proteins that are expressed in some individuals in the population but not others, thereby creating potential antigenic differences between donors and recipients. This occurs, for example, when proteins encoded on the Y chromosome (H-Y) from male grafts induce an anti-Y response in females [3]. In theory, a polymorphism of any protein between donor and recipient, as is the case for certain enzymes and surface receptors that can be processed and presented on self-MHC, can potentially elicit an anti-graft response. Any non-MHC gene that encodes epitopes capable of binding to both MHC class I and class II molecules and inducing both CD4 and CD8 T cell responses can be considered a minor histocompatibility gene. CD8 T cells [4, 5] and, more recently, CD4 T cells [6] specific for minor antigens have been isolated from humans and rodents and have been shown to play an important role in the rejection of solid organs and corneal transplants as well as causing graft-versus-host disease after bone marrow transplantation [3, 7].

    Unique to transplant immunobiology is the idea that alloantigen recognition can occur via two distinct pathways, both of which focus on the source of the antigen presenting cells (donor versus recipient). The direct pathway of allorecognition describes the ability of T cells to “directly” recognize intact non-self MHC molecules present on the surface of donor cells (Fig. 1a). The indirect pathway of allorecognition describes the ability of T cells to recognize donor MHC molecules that are processed and presented as peptides by self-MHC molecules (Fig. 1b). The recognition of intact donor MHC molecule(s) elicits a potent anti-graft immune response while processed MHC peptides and minor histocompatibility antigens elicit a slower tempo, less intense immune response.

    Source : www.ncbi.nlm.nih.gov

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