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• W2060373820 startingPage "5998" @default.
• W2060373820 abstract "The body’s immune system is well known for its capacity to distinguish between self, i.e., the body’s normal tissues, and foreign invaders, such as microorganisms (1). This self versus non-self discrimination is best illustrated by the clinical outcomes of solid tissue transplantation. Donor grafts that are matched to the recipient’s “tissue types” result in successful transplantation, whereas mismatched transplants are rejected. Over the years, immunologists have carefully dissected the intricacies of rejection that is regulated by highly polymorphic (many genes, multiple alleles) molecules encoded in a genetic region termed the major histocompatibility complex (MHC) or HLA complex in humans. Transplant rejection is primarily mediated by T lymphocytes that are also responsible for cell-mediated immunity. T cells can recognize molecules encoded within the MHC, such as MHC class I or class II molecules, and can recognize and be stimulated by foreign MHC molecules, such as on the transplanted tissue, resulting in rejection. In inbred animals, classic transplantation laws were defined by studies of skin grafting. Generally, transplants between two different, MHC-mismatched inbred strains are rejected, whereas MHC-matched transplants are accepted. An F1 hybrid offspring produced by mating of the two inbred strains codominantly expresses MHC alleles from both parents. The F1 hybrid is capable of accepting a transplant from either parent, but each parent rejects F1 hybrid tissue (because it has “foreign” MHC molecules from the other parent). These clear-cut laws even guide clinical transplantation of solid organs in human patients." @default.
• W2060373820 created "2016-06-24" @default.
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• W2060373820 date "1997-06-10" @default.
• W2060373820 modified "2023-09-30" @default.
• W2060373820 title "The mother–child union: The case of missing-self and protection of the fetus" @default.
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• W2060373820 doi "https://doi.org/10.1073/pnas.94.12.5998" @default.
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