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see transplantation, medicaltransplantation, medical,
surgical procedure by which a tissue or organ is removed and replaced by a corresponding part, usually from another part of the body or from another individual.
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A term used to describe the genes that influence acceptance or rejection of grafts. When grafts of tissue are exchanged between genetically dissimilar individuals, profound immunological rejection generally takes place. In contrast, grafts between genetically similar individuals, such as identical twins, are normally tolerated; they are histocompatible. Most known examples of histocompatibility (or H) genes encode polymorphic (that is, tending to differ between individuals) cell-surface proteins.

The major histocompatibility complex (MHC) contains a set of histocompatibility genes, termed major because mismatching at these genes invokes rapid rejection. The main function of MHC genes involves distinguishing self from nonself in the immune system, as part of preventing the spread of infectious disease. The body employs special mechanisms to avoid rejection of the fetus, which is effectively an allograft, that is, a graft from a donor to a genetically dissimilar recipient of the same species; in this case, the mechanisms include a diminution of MHC gene expression.

The MHC contains a spectrum of genes, many of which influence processing and presentation of antigens to the immune system. In mice, the MHC is designated the H-2 complex; in humans, it is referred to as the HLA complex (for human leukocyte A system). Mice and other mammals seem to have a similar arrangement of genes in their MHCs. See Antigen, Cellular immunology, Mendelism, Transplantation biology


The capacity to accept or reject a tissue graft.
References in periodicals archive ?
Class I histocompatibility antigens (HLA-A, B, and C) are expressed on all cells, and class II histocompatibility antigens (HLA-DP, DQ, and DR) are expressed on antigen-presenting cells (B-cells, macrophages, dendritic cells, Langerhans cells, and capillary endothelium).
The antigenic targets of non-HLA antibodies may be minor histocompatibility antigens, vascular receptors, adhesion molecules, and intermediate filaments [8].
If the peptide binding features are not altered, then alloreactive immune reactions are more unlikely; however, they cannot be fully excluded since the genetic variability in the population may give rise to certain minor histocompatibility antigens. The impact of polymorphisms located within the peptide binding region and the risk of severe acute GvHD is well known [10]; furthermore the residues described to impact the risk of GvHD when mismatched (AA 9, 99, 116, 156) have been directly associated with the peptide anchor p2 or pQ [11] or indirectly with peptide binding through differential interaction with the peptide loading complex and peptide selection [12, 13].
Wiley, "The foreign antigen binding site and T cell recognition regions of class I histocompatibility antigens," Nature, vol.