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Immune tolerance in pregnancy or gestational immune tolerance is the absence of a maternal immune response against the fetus and placenta, which thus may be viewed as unusually successful allografts, since they genetically differ from the mother.[1] In the same way, many cases of spontaneous abortion may be described in the same way as maternal transplant rejection.[1]



The placenta functions as an immunological barrier between the mother and the fetus.

The placenta functions as an immunological barrier between the mother and the fetus, creating an immunologically privileged site. For this purpose, it uses several mechanisms:

  • It secretes Neurokinin B containing phosphocholine molecules. This is the same mechanism used by parasitic nematodes to avoid detection by the immune system of their host.[2]
  • Also, there is presence of small lymphocytic suppressor cells in the fetus that inhibit maternal cytotoxic T cells by inhibiting the response to interleukin 2.[1]
  • The placental trophoblast cells do not express the classical MHC class I isotypes HLA-A and HLA-B, unlike most other cells in the body, and this absence is assumed to prevent destruction by maternal cytotoxic T cells, which otherwise would recognize the fetal HLA-A and HLA-B molecules as foreign. On the other hand, they do express the atypical MHC class I isotypes HLA-E and HLA-G, which is assumed to prevent destruction by maternal NK cells, which otherwise destruct cells that do not express any MHC class I.[3] However, trophoblast cells do express the rather typical HLA-C.[3]

Still, the placental barrier is not the sole means to evade the immune system, as foreign fetal cells also persist in the maternal circulation, on the other side of the placental barrier.[4]

One model for the induction of tolerance during the very early stages of pregnancy is the Eutherian Fetoembryonic Defense System (eu-FEDS) hypothesis.[5] The basic premise of the eu-FEDS hypothesis is that both soluble and cell surface associated glycoproteins, present in the reproductive system and expressed on gametes, suppress any potential immune responses, and inhibit rejection of the fetus [6]. The eu-FEDS model further suggests that specific carbohydrate sequences (oligosaccharides) are covalently linked to these immunosuppressive glycoproteins and act as “functional groups” that suppress the immune response. The major uterine and fetal glycoproteins that are associated with the eu-FEDS model in the human include alpha-fetoprotein,CA125, and glycodelin-A (also known as placental protein 14 (PP14)).

However, another model suggests that the induction of tolerance primarily requires the participation of regulatory T cells[7].


Many cases of spontaneous abortion may be described in the same way as maternal transplant rejection.[1] Examples of insufficient immune tolerance in pregnancy are Rh disease and pre-eclampsia:

  • Rh disease is caused by the mother producing antibodies (including IgG antibodies) against the Rhesus D antigen on her baby's red blood cells. It occurs if the mother is Rh negative and the baby is Rh positive, and a small amount of Rh positive blood from any previous pregnancy has entered the mother's circulation to make her produce IgG antibodies against the Rhesus D antigen. Maternal IgG is able to pass through the placenta into the fetus and if the level of it is sufficient, it will cause destruction of Rhesus D positive fetal red blood cells leading to development Rh disease. Generally Rhesus disease becomes worse with each additional Rhesus incompatible pregnancy.


If the mechanisms of rejection-immunity of the fetus could be elucidated, it could avail for xenopregnancy, having, for example pigs carry human fetuses to term as an alternative to a human surrogate mother, providing a sober, drug-free and nonsmoking carrier.[10]


  1. ^ a b c d Clark DA, Chaput A, Tutton D (March 1986). "Active suppression of host-vs-graft reaction in pregnant mice. VII. Spontaneous abortion of allogeneic CBA/J x DBA/2 fetuses in the uterus of CBA/J mice correlates with deficient non-T suppressor cell activity". J. Immunol. 136 (5): 1668–75. PMID 2936806.  
  2. ^ "Placenta 'fools body's defences'". BBC News. 2007-11-10.  
  3. ^ a b Page 31 to 32 in: Maternal-Fetal Medicine : Principles and Practice. Editor: Robert K. Creasy, Robert Resnik, Jay D. Iams. ISBN: 9780721600048 Published: September 2003
  4. ^ Williams Z, Zepf D, Longtine J, et al. (March 2008). "Foreign fetal cells persist in the maternal circulation". Fertil. Steril.. doi:10.1016/j.fertnstert.2008.02.008. PMID 18384774.  
  5. ^ Clark, Clark G.F., Dell A., Morris H.R., Patankar M.S., and Easton R.L. (2001) The species recognition system: a new corollary to the human fetoembryonic defense system hypothesis. Cells Tissues Organs 168, 113-21 PMID 11114593
  6. ^ Clark, G. F., Dell, A., Morris, H. R., Patankar, M. S. and Easton, R. L. (2001) The species recognition system: a new corollary for the human fetoembryonic defense system hypothesis. Cells Tissues Organs. 168, 113-21. PMID 11114593
  7. ^ Trowsdale J, and Betz AG. 2006. Mother's little helpers: mechanisms of maternal-fetal tolerance. Nature Reviews Immunology 7:241-6 PMID 16482172
  8. ^ Sarah Robertson. "Research Goals --> Role of seminal fluid signalling in the female reproductive tract".  
  9. ^ Sarah A. Robertson, John J. Bromfield, and Kelton P. Tremellen (2003). "Seminal ‘priming’ for protection from pre-eclampsia—a unifying hypothesis". Journal of Reproductive Immunology 59 (2): 253–265. doi:10.1016/S0165-0378(03)00052-4.  
  10. ^ Darwin's children LeVay, Simon. (1997, October 14). from The Free Library. (1997). Retrieved March 06, 2009


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