Eutherian fetoembryonic defense system hypothesis

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The eutherian fetoembryonic defense system (eu-FEDS) is a hypothetical model describing a method by which immune systems are capable of recognizing additional states of relatedness like "own species" such as is observed in maternal immune tolerance in pregnancy. The model includes descriptions of the proposed signaling mechanism and several proposed examples of exploitation of this signaling in disease states.

Background

The concept of

autoimmune disorders
.

The term Eutheria is a taxon describing placental organisms such as mammals. The sister group of Eutheria is Metatheria, which includes marsupials and their extinct relatives.

The term eu-FEDS was first described in 1997 by Gary F. Clark et al.

IVF).[3] The eu-FEDS hypothesis was itself proposed to describe the precise immunological
mechanisms that mediate protection of the developing eutherian fetus from the immune responses of its mother.

Hypothesis

The basic premise of the eu-FEDS hypothesis is that both soluble and cell surface associated

CA125
, and glycodelin-A (also known as placental protein 14 (PP14)).

Normally, a low level of these glycoproteins is detected in the maternal

immunosuppressive effect of these glycoproteins may be so complete that their continued leakage into the circulatory system
could lead to a global suppression of the maternal immune response, compromising the mother's ability to carry the fetus to term.

Implications of the hypothesis

Human

NK cells. These cells target and kill other cells lacking such MHC markers, a concept known as "missing self".[7] One distinct possibility is that sperm and eggs are recognized via oligosaccharides expressed on their surfaces. For example, human gametes are coated with carbohydrate sequences that have been implicated in the suppression of NK cell mediated responses.[8]

One of the major

stomach ulcers
.

There are some notable examples of this mimicry or acquisition of the same carbohydrate sequences implicated in this protective system by pathogens and aggressive tumor cells. The major carbohydrate sequence linked to glycodelin-A also profusely coats the surface of schistosomes.

gp120) almost perfectly overlap.[11] More persistent pathogens linked to the eu-FEDS model may be identified as mass spectrometry
methods for sequencing oligosaccharides become more sensitive.

Other experimental models

Several other models have been developed that seek to address this hypothetical system for immune tolerance, including the depletion of tryptophan via the enzyme indoleamine dioxygenase (IDO)[12] and the expression of the nonclassical MHC class I molecule designated HLA-G.[13] However, genetic deletion of IDO in female mice does not lead to the rejection of their foreign fetal offspring,[14] indicating that a redundant system for the suppression of the mother's immune response exists in the uterus during pregnancy. In addition, HLA-G expresses oligosaccharides that are very different from those linked to other HLA class I molecules,[15][16] so the possibility exists that HLA-G at the fetomaternal interface is itself employing its unusual carbohydrate sequences as functional groups to suppress the mother's immune response.

See also

References

  1. ^
    PMID 11114593
    .
  2. ^ Medawar, P. (1953). "Some immunological and endocrinological problems raised by the evolution of viviparity in vertebrates". Symp. Soc. Exp. Biol. VII: 320–338.
  3. PMID 6398696
    .
  4. PMID 9730286
    .
  5. PMID 13689158
    .
  6. PMID 2002651
    .
  7. PMID 2201309
    .
  8. PMID 9239739
    .
  9. PMID 9239703
    .
  10. PMID 7592613
    .
  11. PMID 12734200
    .
  12. PMID 9712583
    .
  13. PMID 16972895
    .
  14. PMID 15063630
    .
  15. PMID 9637505
    .
  16. PMID 8617950
    .
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