Minor histocompatibility antigen (also known as MiHA) are peptides presented on the cellular surface of donated organs that are known to give an immunological response in some organ transplants.[1] They cause problems of rejection less frequently than those of the major histocompatibility complex (MHC). Minor histocompatibility antigens (MiHAs) are diverse, short segments of proteins and are referred to as peptides. These peptides are normally around 9-12 amino acids in length and are bound to both the major histocompatibility complex (MHC) class I and class II proteins.[2] Peptide sequences can differ among individuals and these differences arise from SNPs in the coding region of genes, gene deletions, frameshift mutations, or insertions.[3] About a third of the characterized MiHAs come from the Y chromosome.[4] Prior to becoming a short peptide sequence, the proteins expressed by these polymorphic or diverse genes need to be digested in the proteasome into shorter peptides. These endogenous or self peptides are then transported into the endoplasmic reticulum with a peptide transporter pump called TAP where they encounter and bind to the MHC class I molecule. This contrasts with MHC class II molecules's antigens which are peptides derived from phagocytosis/endocytosis and molecular degradation of non-self entities' proteins, usually by antigen-presenting cells. MiHA antigens are either ubiquitously expressed in most tissue like skin and intestines or restrictively expressed in the immune cells.[5]
Minor histocompatibility antigens are due to normal proteins that are in themselves polymorphic in a given population. Even when a transplant donor and recipient are identical with respect to their major histocompatibility complex genes, the amino acid differences in minor proteins can cause the grafted tissue to be slowly rejected.
Several of the identified Autosomally and Y chromosome encoded MiHAs[4]
^Robertson NJ, Chai JG, Millrain M, Scott D, Hashim F, Manktelow E, Lemonnier F, Simpson E, Dyson J (March 2007). "Natural regulation of immunity to minor histocompatibility antigens". Journal of Immunology. 178 (6): 3558–65. doi:10.4049/jimmunol.178.6.3558. PMID 17339452.
^Dzierzak-Mietla M, Markiewicz M, Siekiera U, Mizia S, Koclega A, Zielinska P, Sobczyk-Kruszelnicka M, Kyrcz-Krzemien S (2012). "Occurrence and Impact of Minor Histocompatibility Antigens' Disparities on Outcomes of Hematopoietic Stem Cell Transplantation from HLA-Matched Sibling Donors". Bone Marrow Research. 2012: 257086. doi:10.1155/2012/257086. PMC 3502767. PMID 23193478.
^Linscheid C, Petroff MG (April 2013). "Minor histocompatibility antigens and the maternal immune response to the fetus during pregnancy". American Journal of Reproductive Immunology. 69 (4): 304–14. doi:10.1111/aji.12075. PMC 4048750. PMID 23398025.
^ abHirayama M, Azuma E, Komada Y (2012). Major and Minor Histocompatibility Antigens to Non-Inherited Maternal Antigens (NIMA), Histocompatibility. INTECH. p. 146. ISBN 978-953-51-0589-3.
^Bleakley M, Riddell SR (March 2011). "Exploiting T cells specific for human minor histocompatibility antigens for therapy of leukemia". Immunology and Cell Biology. 89 (3): 396–407. doi:10.1038/icb.2010.124. PMC 3061548. PMID 21301477.
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