الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
The human leukocytic antigen system (HLA) is the name of the major histocompatibility complex (MHC) in humans. The superlocus contains a large number of genes related to immune system function in humans. This group of genes reside on chromosome 6, and encode cell-surface antigen-presenting proteins and many other genes. The HLA genes are the human versions of the MHC genes that are found in most vertebrates. The proteins encoded by certain genes are also known as antigens, as a result of their historic discovery as a factors in organ transplantations. The major HLA antigens are essential elements for immune function. The HLA genes are classified into three classes: HLA class I antigens (A,B&C) present peptides from inside the cell, HLA class II antigens present antigens from outside of the cell to T-lymphocytes & HLA class III antigens encode components of the complement system. HLA antibodies are typically not naturally occurring, with few exceptions are formed as a result of an immunologic challenge of a foreign material containing non-self HLAs via blood transfusion and organ or tissue transplant. Anti-HLA antibodies may be detected as early as a few days following transplantation or after several years and expansion of humoral donor-specific alloreactivity to more than one mismatched molecule during the post-transplant period may be useful for the identification of those patients at risk of losing graft function or rejection . Anti-HLA antibodies are responsible for the different forms of antibody-mediated histological changes. Detection of HLA antibodies by CDC, flow cytometry,ELISA and Luminex antibody screening technology. Acute and chronic allograft rejection can occur in HLA-identical sibling transplants implicating the importance of immune response against non-HLA targets. Non-HLA antibodies may occur as alloantibodies, yet they seem to be predominantly autoantibodies. Antigenic targets of non-HLA antibodies described thus far include various minor histocompatibility antigens, vascular receptors, adhesion molecules, the major histocompatibility complex class I chain-related gene A (MICA) or MICB, or tissue-specific autoantigens such as vimentin, cardiac myosin (CM), collagen V (Col V), agrin , angiotensin II receptor type I (AT1) , Anti-ICAM-1 IgM , perlecan, Anti-GBM antibodies and K-α1 tubulin. The aim of the present work is to demonstrate the value of HLA and non HLA antibodies in organ transplantation and its outcome. We attempted to summarize the current state of research, development in diagnostic and therapeutic strategies, and to address some emerging problems in the area of humoral response against non-HLA antigens beyond ABO blood group and MHC class I chain-related gene A and B antigens in solid organ transplantation . In summary, matching in organ transplantation has evolved over the years to a very refined and sophisticated series of tests. These tests better assure that any donor organ will have the best possible chance of helping the recipient for whom it is intended. Further refinements in crossmatching are always on the horizon, and there are special situations, even regarding blood type matching, which certain transplant centers are attempting to improve. This is also true of tissue typing and its related antibody production, which prevents transplantation in some cases and even applies to the positive crossmatch between the donor and recipient, something that certain centers are attempting to address. On balance, however, a well matched organ is one in which the blood type between the donor and recipient are compatible, the tissue typing well defined and hopefully well matched and all crossmatch studies are negative. Application of good matching studies in clinical organ transplantation has allowed for excellent results using living donor and cadaveric organs and has permitted safe organ transplantation for thousands of patients with end-stage organ failure. For the vast majority of the 51 yr since the first organ transplant, T cell–mediated inflammation was believed to be the central process in allograft rejection. Therapies to prevent and treat allograft rejection consequently have been directed primarily against T cells. Improvements in these drugs have led to greatly improved rates of acute cellular rejection and 1-yr graft survival; however, acute rejection does still occur, as does long-term chronic rejection. It was the development of the immunohistochemical process for visualization of complement split product C4d in graft tissue that first provided concrete evidence linking antibody binding and complement activation in renal allografts to the mechanism by which damage occurs in this setting . We now recognize that alloantibodies play a role in rejections that do not respond to T cell therapies and, indeed, require targeted therapies that address the various mechanisms by which they exert their effects. Newer, more sensitive technologies for serum antibody screening are allowing for clearer delineation of the relationship between antibodies and acute and chronic allograft pathologies and their attendant clinical outcomes. * Donor specific HLA antibodies are involved in transplant rejection, they are an absolute contraindication for organ transplantation several years ago. The old dogma is now destroyed with the advent of immunosuppressive therapies. Non HLA antibodies continues to evolve in complexity and still raises many questions . Severe injuries may develop in organs of recipients at particular risk due their presence.