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Macrophages rejection

Type IV Reactions Also termed delay-type hypersensitivity reaction, these take 48-72 h to develop and are not antibody-mediated. Antigens are recognized by CD4+ and/or CD8+ cells in the context of MHC class restrictions on APCs. These reactions are T-cell-mediated where activated T cells release cytokines, resulting in the development of granulomas from macrophages. These mechanisms are responsible for symptoms that may include transplant rejection, contact dermatitis, leprosy, tuberculosis and sarcoidosis. [Pg.129]

Fig. 7.1 Phases of tissue transplant rejection. The transplanted tissue sheds antigens. These antigens undergo uptake, processing and presentation to the T cells in the secondary lymphoid tissue by APCs, which include macrophages, B cells, Langerhans cells or dendritic cells. This phase results in the production of antibodies and antigen-specific TH and Tc cells. The antibodies and effector cells then migrate to the grafted tissue where TH cells secrete cytokines and which in combination with the antibodies and Tc cells destroy the grafted tissue (see Color Insert)... Fig. 7.1 Phases of tissue transplant rejection. The transplanted tissue sheds antigens. These antigens undergo uptake, processing and presentation to the T cells in the secondary lymphoid tissue by APCs, which include macrophages, B cells, Langerhans cells or dendritic cells. This phase results in the production of antibodies and antigen-specific TH and Tc cells. The antibodies and effector cells then migrate to the grafted tissue where TH cells secrete cytokines and which in combination with the antibodies and Tc cells destroy the grafted tissue (see Color Insert)...
About 10 days after transplantation, acute rejection of the graft begins as a result of cell-mediated immunity. Acute rejection is a result of infiltration of large numbers of macrophages and lymphocytes into the graft. Helper T-cell activation and proliferation play a major role in this process, and both complement-dependent cell-mediated cytotoxicity and ADCC are involved in the destruction of the graft. Acute rejection could be in the form of acute vascular rejection, acute cellular rejection or both. Acute vascular rejection involves the necrosis of the blood vessel cells of the graft... [Pg.154]

Acute cellular rejection involves infiltration of macrophages and lymphocytes into the graft and is evident from the necrosis of the parenchymal cells of the graft. The lysis of the parenchymal cells of the transplanted tissue is achieved by the infiltrating leukocytes. Acute cellular rejection may be the product of several mechanisms including cytolytic T-cell-mediated lysis, NK cell-mediated lysis and activated macrophage-mediated lysis. The acute cellular rejection predominantly involves CD8+ T cytolytic cells that kill the grafted tissue. [Pg.155]

Astralagus 2. Echinacea 3. Liquorice 4. Milk thistle 5. Neem 6. Sea buckthorn 1. Ciclosporin 2. Azathioprine 3. Methotrexate 4. Tacrolimus 5. Dadizumab 6. Cyclophosphamide Possibility of graft rejection 1 blood level unknown mechanism (astralagus). Other mechanisms alkyl amides from echinacea modulate tumour necrosis factor alpha mRNA expression in human monocytes/macrophages via the cannabinoid type 2 receptor Unknown mechanism (milk thistle is known to l cyclosporine levels neem L effects of azathioprine, prednisolone and dadizumab sea buckthorn may 1 effect of cyclophosphamide) Induces metabolizing enzymes, CYP3A4 and P-gp (St John s wort L ciclosporin and tacrolimus levels) Avoid concomitant use of the herb... [Pg.747]

JoseMD, Ikezumi Y,Van Rooijen N, Atkins RC, Chadban SJ Macrophages act as effectors of tissue damage in acute renal allograft rejection.Transplantation 76 1015-1022,2003... [Pg.208]


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