The KIRs with short and long cytoplasmic domains are activating and inhibitory receptors and transduce their signals through DAP-12 and tyrosine-based motifs, respectively. graft is taken and transplanted from different parts of the same individual. The processes of transferring grafts between genetically identical and nonidentical individuals of the same species are known as isograft and allograft transplantation, respectively. In contrast, xenograft refers to the transplantation of grafts between two different species such as from baboon to human. Implantation of human Rabbit Polyclonal to LAMA5 cancer cells in mice for tumour study is also assumed to be xenograft transplantation[3,4]. The current practice of allograft transplantation is to have as many match for ABO and human leukocyte antigen (HLA) loci as possible between the donor and recipient. However, this is not the case for isograft and autograft as the transplanted graft originated from the genetically identical resources. Incompatibility between donor and recipient will cause rejection since the graft will be considered as nonself by the recipients immune surveillance and the rate of graft rejection will vary depending on time courses, types of tissue or organ grafted and the immune responses involved. REJECTION AND GRAFT HOST DISEASE In general, there are three types of graft rejections, the production of cytokines and alloantibodies which activate the classical pathway of complement system[19,20]. However, the actual mechanism of this rejection is not very well understood. It is usually characterized by fibrosis and arteriosclerosis, due to extensive proliferation of smooth muscle cells. Repairing process of damaged tissues and macrophages activation in chronic rejection can lead to fibrosis formation[21-23]. The transplanted allograft can also trigger immune reactions [host disease Goserelin (GVHD)] against mismatched antigens possessed by the recipients. The GVHD is predominantly occurs in bone marrow transplantation which involves alloreactivity of donors lymphocytes against the incompatible tissues of the immune-suppressed host [8]. However, improved outcomes were observed in haplo-identical (leukaemia effect) against the cancerous cells after haplo-identical stem cell transplantation[27-29]. The inhibitory and alloreactivity of NK cells are determined by HLA molecules which acting as ligands (Table ?(Table1)1) for their immunoglobulin-like receptors [and alleles) on the long arm of chromosome 9. The co-dominant and alleles differ by four nucleotide substitutions (C526G, G703A, C796A and G803C) while the ?261G deletion differentiates between the recessive and alleles[83-85]. The 1,3-N-acetylgalactosaminyltransferase encoded by allele and 1,3-D-galactosyltransferase encoded by alleles then convert H antigens, the products of gene located on human chromosome 19 to either A or B antigens, respectively[86]. In contrast, there is no enzymatic activity on H antigen for those bearing the allele due to the ?261G deletion on the background of allele. Thus, the A, B, O and AB phenotypes are determined by the three ABO allelic variants; and alleles. HLA The HLA class I molecules consist of a non-polymorphic 2-microglobulin and a highly polymorphic -chain glycoprotein encoded by the genes within MHC on the chromosome 6[87-89]. There are three types of HLA class I molecules (A, C and B) with their specificities depend on the polymorphic -chain encoded by and genes in the classical class I sub-region of MHC[90]. In contrast, both – and -chains of class II HLA molecules (DP, DQ and DR) are encoded by genes in the classical class II sub-region of MHC[12] (Figure ?(Figure2).2). The class I and II gene clusters within MHC are separated by the class III sub-region which codes for complement components and not part of endogenous and exogenous peptide presentation to CD8+ and CD4+ cells, respectively[91-93] (Figure ?(Figure11). The World Health Organization has developed an alphanumeric nomenclature to name antigens, genes and alleles (Figure ?(Figure3).3). This systematic alphanumeric nomenclature begins with letters representing specific gene and followed by an asterisk and two sets of digits specific for allele group and glycoprotein. Two additional sets of digits are then used to specify synonymous nucleotide changes and mutation outside the non-coding region, respectively. Suffixes (alleles[12,94]. Open in a separate window Figure 3 Systematic human leukocyte antigen nomenclature developed by the World Health Organization Nomenclature Committee for Factors of the human leukocyte antigen system. HLA: Goserelin Human leukocyte antigen. MICA The MICA molecules are stress induced antigens encoded by Goserelin a gene within MHC region (Figure ?(Figure2)2) and are expressed by a wide range of cells including monocytes, keratinocytes and fibroblasts[14,87,95-97]. Unlike HLA class I molecule, MICA is not linked to 2-microglobulin and NK cells and CD8+ T ( and ) cells reactivity are stimulated through interaction of MICA and its ligand, the NKG2D receptor[13-15,98]. Variants of gene are largely.