Is restricted antigen presentation the explanation for fetal allograft survival?

GW Wood - Immunology Today, 1994 - cell.com
GW Wood
Immunology Today, 1994cell.com
Mammalian embryos express paternal histocompatibility antigens which make tbem
potential targets for the maternal immune system. The trophoblast is a major
histocompatibility complex (MHC) antigennegative barrier between mother and fetus which
facilitates movement of antigenic molecules but prevents traffic of antigenic cells and is itself
unable to present an,: igen. Gary Wood svggests that the lack of antigen presentation
requirements for MHC class I-restricted T-cell responses prevent generation of paternal …
Mammalian embryos express paternal histocompatibility antigens which make tbem potential targets for the maternal immune system. The trophoblast is a major histocompatibility complex (MHC) antigennegative barrier between mother and fetus which facilitates movement of antigenic molecules but prevents traffic of antigenic cells and is itself unable to present an,: igen. Gary Wood svggests that the lack of antigen presentation requirements for MHC class I-restricted T-cell responses prevent generation of paternal-antigen directed cell-mediated immunity.
Mammalian reproduction is initiated by the ma,: ing of individuals with distinct genotypes, Polymorphism of histocompatibility antigens is one expression of that genetic individuality. The cellular immune responses that are responsible for rejection of tissue grafts between individuals are directed toward those polymorphic antigens. Tissue rejection responses are mediated by major histocompatibility complex (MHC) class I-restricted CD8÷ T cells produced with help from MHC class lI-restricted CD4* T lymphocytes. The conceptus expresses both maternally and! caternallyderived histocompatibility antigens during development TM. Production of histocompatibility antigenspecific antibodies during normal pregnanc~ in most, if not all, mammalian species> 8 demonstrates that fetal cells express the antigens in a form that ailows recognition by maternal T and B cells, since antibody production b~ B cells is dependent on MHC class II-restricted CD4÷ T cells. Although fetal cell-associated histocompatibility antigens have the potential to stimulate cellmediated immune responses 9'm, no such response l: as been documented in any species during normal or abnormal pregnancy. It, this regard, it is important to emphasize that identifying cytotoxic T lymphocyte (CTL) respen,~ e~ involves more than killing of alloantigen positive targets. Specificity of the effector cells must be established. Moreover, if CTL are present in
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