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Histocompatibility genes control the production of proteins on the outer membranes of tissue and blood cells, especially lymphocytes, and are essential elements in cell-cell recognition and interaction. Surface proteins also determine the level and type of immune response, are involved in the presentation of antigens to the immune system, and may serve other biochemical and immunologic functions. In human beings, proteins encoded by multiallelic genes of the major histocompability complex (MHC) on chromosome 6 are known as human leukocyte antigens (HLA). MHC molecules are divided into two classes on the basis of distinctive polypeptide subunits and biologic function. Class I MHC molecules, which are found on all nucleated cells, consist of an α chain (45 kD) and a small peptide called β2-microglobulin (12 kD). They are involved in presentation of antigens to cytotoxic (CD8) lymphocytes. Class II MHC molecules consist of an α chain (30-34 kD) and a β chain (26-29 kD). They are expressed by all B lymphocytes, interdigitating dendritic cells, and thymic epithelial cells. Other cells, including T lymphocytes, macrophages, and endothelial cells, can be induced by cytokines to express them. They function in presenting antigen to CD4 helper lymphocytes. Class I MHC molecules are encoded by HLA-A, HLA-B, and HLA-C genes; class II MHC molecules by HLA-D (DP, DQ, DR) genes. In the case of allografts, the greater the histocompatibility (that is, the closer the match between donor and recipient cell surface antigens), the less is the likelihood of rejection. HLA typing of a potential marrow donor and a potential transplant recipient is used to predict graft rejection and graft-versus-host disease. The possession of certain allelic HLA genes predisposes to specific diseases. For example, the HLA-B27 allele is found in 90% of patients with ankylosing spondylitis; HLA-DR4 is associated with rheumatoid arthritis, HLA-DR2 with both Goodpasture syndrome and multiple sclerosis. The association of HLA alleles with specific diseases has prompted speculation that some infectious agents may use HLA molecules to gain access to host cells, may mimic HLA molecules so as to be recognized as self by T cells, or may combine with certain HLA molecules to form a complex not recognized at all by T cells.