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The Host Response to Grafts and Transplantation Immunology
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Cytolytic T lymphocytes are generated in vitro in mixed lymphocyte cultures. Like the graft-reactive lymphocytes from the thoracic ducts of grafted animals, the cytotoxic lymphocytes that develop in mixed lymphocyte cultures can only lyse cells that display the alloantigens present on the stimulator cells. These cytotoxic lymphocytes are thus alloantigen specific. When a lymphocyte population is cultured with foreign cells, only a fraction of the lymphocytes in the population develop cytolytic activity, specifically, those lymphocytes with antigen receptors that can recognize the foreign histocompatibility antigens. The other lymphocytes are not stimulated and do not become lytic cells.
Autoimmunity and Rheumatic Fever
Published in Irun R. Cohen, Perspectives on Autoimmunity, 2020
The most important study concerning the possible role of a haplotype related to rheumatic predisposition is the demonstration of a B-cell alloantigen (designated 833) that was found in 75% of rheumatic patients in one study.35 The same alloantigen was present in 16.5% of a population of normal individuals. Adequate control groups of other chronic inflammatory diseases were not included. The alloantigen could not be correlated with a known specificity in the mixed lymphocyte culture and was not associated with any known HLA-A, -B, or -D antigens. In an extension of these studies employing monoclonal mouse hybridoma reagents with 883 allospecificity, relative segregation was recorded for 833-positive B-cell typing among rheumatic heart patients in India, New Mexico, and New York, respectively, as compared to normal unaffected controls.30 Again, however, other chronic inflammatory disease groups were not included as control populations nor was there a clear attempt to distinguish differences among RF subjects with and without rheumatic heart disease or heart disease of varying severity. The same investigators found this B-cell alloantigen to be physically distinct from, but close to, sites on antigen-reactive B-cells that actually bind to group A streptococcal membrane antigens.36 Perhaps further experimental work might clarify more specifically the B-cell alloantigens that appear to be associated with rheumatic subjects.
Immunologic Tolerance
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
The administration of donor alloantigen to a graft recipient may induce tolerance to the grafted tissue. Blood is the material most often used, since it is a readily available and easily administered source of alloantigen. Bone marrow has also been used, and may be superior for tolerance induction due to its content of stem cells, and the potential to establish hematologic chimerism and the persistence of donor antigen outside the graft. A multitude of protocols have been used, almost all of them using donor immunization in conjunction with an immunosuppressive treatment, such as cyclosporine et al., anti-lymphocyte antibodies, or irradiation. These combination therapies have proven quite effective in prolonging graft survival.
Applications of Transcriptomics in the Research of Antibody-Mediated Rejection in Kidney Transplantation: Progress and Perspectives
Published in Organogenesis, 2022
The formation of DSA results in three following consequences: complement-dependent cytotoxicity, antibody-dependent cellular toxicity, and direct endothelial injury.13 Upon the binding of DSA to alloantigen, the classical complement pathway is activated, which produces anaphylatoxins including C3a and C5a, recruits inflammatory cells, and ultimately leads to tissue injury.14 During this process, C4d is produced as a degradation product that binds to the endothelial basement membrane and appears as an in situ marker of complement activation in renal allografts.15 The Fc receptor binding to the Fc of innate immune cells including macrophages and natural killer (NK) cells is responsible for antibody-dependent cellular toxicity and leads to degranulation, cell lysis, and phagocytosis.14 The direct binding of the antigens on allograft endothelial cells also causes endothelial activation and proliferation. Instead of being a passive victim, the endothelial cells also participate in the pathogenesis of rejection including leukocyte adhesion and recruitment, lymphocyte activation and differentiation, as well as the secretion of cytokines and chemokines after activation.16
Design and Optimization of PLGA Particles to Deliver Immunomodulatory Drugs for the Prevention of Skin Allograft Rejection
Published in Immunological Investigations, 2020
Khawar Ali Shahzad, Muhammad Naeem, Lei Zhang, Xin Wan, Shilong Song, Weiya Pei, Chen Zhao, Xiaoxiao Jin, Chuanlai Shen
Major barrier in the process of alloskin graft transplantation is the recognition of donor alloantigens by the host immune system (Hlavaty et al. 2015). The graft rejection is initiated by the CD8+ effector T cells of major histocompatibility complex (MHC) class I, which are present on the surface of all nucleated cells (Benichou 1999; Den Haan et al. 2000; Fehres et al. 2014; Shah et al. 2019a). The peptides of donor alloantigen are presented on the surface of presented by APCs that are more prevalent than antigen-specific T cells for other foreign antigens (Masri 2003; Suchin et al. 2001). The accumulation of donor antigens results in skin allograft rejection by host immune system either directly via alloantigen recognition of the donor or indirect alloantigen recognition of recipient MHC molecules (Hess et al. 2007; Shilling and Wilkes 2009). Hence, the accumulation of donor alloantigens is liable to allograft rejection, which is difficult to control.
TNFR2: The new Treg switch?
Published in OncoImmunology, 2018
José L. Cohen, Kathryn J. Wood
This concept that donor T cells play a critical role is supported by the observed increased risk of leukemia relapse when T cells with alloreactivity are reduced or absent as occurs with autografts, syngeneic twin grafts or with T cell depleted allogeneicSCT.8 However, the infusion of donor T cells is regarded as a double edged sword as the major drawback of this beneficial alloreactive effect on GVL/GVT is an increased risk of GVHD. Depending on the HLA disparity between donor and recipient, alloreactive T cells represent approximately 5–10% of the T cell repertoire present in healthy individuals.9 When donor T cells are infused into an allogeneic recipient, they undergo activation in response to host alloantigen presenting cells (APC), proliferate and differentiate into cytokine-producing and cytotoxic effectors T cells that have the potential to cause tissue damage in target organs. In order to reduce the risk and prevent GVHD, grafted patients receive immunosuppressive drug therapy but this treatment is only partially effective.7