why human body does not develop immune reaction to the fetus?

Answer 1

There was an interesting article a few years ago in the New England Journal of Medicine regarding fetal cells and scleroderma. Scleroderma is a rare disease that usually affects females who have had kids. The disease is characterized by thickening and hardening of the skin in its most benign form. The theory suggest that during birth some fetal cells are released into the mother's blood and get embedded into their face or fingers. As time goes on, the mother's immune system attacks these fetal cells and as the theory suggest a chronic host vs graft reaction occurs. I thought it was sort of interesting.

Answer 2

Actually, it does develop an immune reaction to the fetus - this is what causes "morning sickness". Eventually, however, if the pregnancy is not abnormal, the body will realize that the fetus is not an attacking invader, and the reaction will stop.

Answer 3

The fetus is not a disease or virus,so it does not trigger the immune system.The fetus has the same biology that the mother does....usually-only if the child has a different Rh (Chemical difference) from the mother does the mother risk having an immune response and two different types of blood would be in the same body,sicking one of them.

Answer 4

This is a great question and the focus of much research. Implantation is similar to an organ transplant. It seems that the immune system has mechanisms that are tolerogenic that allow for fetal ingraftment - some of these mechanisms prevent the development of autoimmune diseases - which maybe why during pregancy some diseases are alieviated.

Answer 5

why human body does not develop immune reaction to the fetus?

Answer: Because of the presence of Blood Placental Barrier. Only Immunoglobulin G (IgG) can pass through the barrier.
(note: we have several types of IG...such as IgG, IgA, IgM, IgE)
But i can give you a good example of immune reaction to fetus.

Have you heard of HEMOLYTIC DISEASE OF THE NEWBORN - Rh Incompatibility?

Rh incompatibility can occur by two main mechanisms. The most common type occurs when an Rh-negative pregnant mother is exposed to Rh-positive fetal red blood cells secondary to fetomaternal hemorrhage during the course of pregnancy from spontaneous or induced abortion, trauma, invasive obstetric procedures, or delivery. Rh incompatibility can also occur when an Rh-negative female receives a blood transfusion that contains Rh antigens. In part, this is the reason that blood banks prefer using blood type "O-negative" or "type-O, Rh negative," as the universal donor type, especially in females.

The most common cause of Rh incompatibility is exposure to an Rh-negative mother by Rh-positive fetal blood during pregnancy or delivery, whereby red blood cells from the fetal circulation leak into the maternal circulation. After a significant exposure, sensitization occurs and maternal antibodies are produced against the foreign Rh antigen.

Once produced, maternal Rh immunoglobulin G (IgG) antibodies may cross freely from the placenta to the fetal circulation, where they form antigen-antibody complexes with Rh-positive fetal erythrocytes and eventually are destroyed, resulting in a fetal alloimmune-induced hemolytic anemia. Although the Rh blood group systems consist of several antigens (eg, D, C, c, E, e), the D antigen is the most immunogenic; therefore, it most commonly is involved in Rh incompatibility.

The risk and severity of sensitization response increases with each subsequent pregnancy involving a fetus with Rh-positive blood. In women who are prone to Rh incompatibility, the second pregnancy with an Rh-positive fetus often produces a mildly anemic infant, whereas succeeding pregnancies produce more seriously affected infants who ultimately may die in utero from massive antibody-induced hemolytic anemia.

Causes: (usually disruption of Blood Placental Barrier)
Ectopic pregnancy
Placenta previa
Placental abruption
Abdominal/pelvic trauma
In utero fetal death
Any invasive obstetrical procedure (eg, amniocentesis)
Lack of prenatal care
Spontaneous abortion


I hope this one is helpful to you...

Answer 6

"Toxemia of pregnancy " is a type of immune reaction to incompatible fetus."Spontaneous abortions" also occur as a result of "incompatible fetus".

Answer 7

dont know exactly but i would think that it knows when it is a healthy fetus or an irregular one. in the latter case, miscarriages happen

Answer 8

http://www.cnn.com/HEALTH/9808/21/fetal.rejection/

Answer 9

In some women the immune system does react to the fetus. Doctors beleive that a lot of repeated unexplained misscarrages are when the women's immune system overreacts and sends NK Cells to hunt down any forign body(the fetus) and kill it. That can be calmed down sonetines with steroids.

British scientist ‘excited’ by miscarriage study –
another false dawn

On further reading, it appears that Dr Siobhan Quenby (Liverpool University) has given patients a steroid, which suppresses the immune system, as scientists believe, ‘an overreaction of the immune system may lead a woman’s body to attack a developing embryo and thus terminate the pregnancy.’ The results, at first glance, appear exciting.

Dr Quenby is quoted as saying, ‘So many women feel doctors are brushing them off because they say there is nothing they can do. The fact that we are trying something gives them real hope. Without this, they would simply have no options.’

As the author of A New Dawn, I take exception to Dr Quenby’s comments for two reasons. Firstly, Dr Quenby is offering women a steroid that, according to The State of California, Environmental Protection Agency (August 20, 1999), is ‘known to cause cancer or reproductive toxicity’ (my emphasis). The steroid in question is Prednisalone.

This may appear perverse by my second charge is even more important, I believe that Dr Quenby is guilty of ‘dereliction of duty’ in her rush to expose desperate women to a known hostile agent. The first step in any research project, having determined the subject to be researched, is a literature search. Before the Internet became available, this was a tortuous undertaking requiring hours, if not weeks, searching through micro-fiche copies of the learned journals, today it takes a couple of ‘key-words’ and ten minutes on Pubmed or any of the other medical search engines.

Had Dr Quenby and her team bothered with this scientific nicety they would have discovered that their work is, in fact, far from a ‘breakthrough’, that the ‘overreaction of the immune system’ has been mapped (and is far more comprehensive than they appear to appreciate) and that women do have options that can be exercised before they are encouraged to take Prednisalone, options that address each of the four major pathways by which inflammation threatens miscarriage – making miscarriage, recurrent or not, entirely preventable. A simple literature search would also have revealed that inflammation also underwrites infertility, PCOS, pre-eclampsia and prematurity.

As I say in A New Dawn (p29), ‘sadly, when presented with compelling evidence, modern medicine normally looks forward to a pharmaceutical treatment rather than backwards to cause.’ Prednisalone is so obviously not a drug of choice for those who suffer miscarriage that its use beggars belief. Do not take my word for it, www.rxlist contains a horrifying catalogue of warnings and known side effects including (but not exclusively):

an immediate warning should curtail any interest if it is read in context. Women of childbearing age invariably mix with other women with young children, thus exposing themselves to chicken pox and measles – these can be fatal if contracted while taking Prednisalone! As if that were not enough the drug can enhance the effects of hypothyroidism and cirrhosis. It can induce mood swings, personality changes, severe depression and frank psychotic manifestations. Anyone with ulcerative colitis should take care as ulcer perforation risk is increased. Recorded side effects include sodium retention, fluid retention, congestive heart failure, potassium loss, hypertension, pancreatitis, latent diabetes and decreased carbohydrate tolerance and convulsions. Menstrual irregularities, headaches, increased sweating and abdominal distention only add to the misery.

Is this yet another false dawn for those who suffer so much? The answer is, ‘no’. Dr Quenby has the right diagnosis, merely the wrong treatment.

In A New Dawn, I report on four different ways in which inflammation causes miscarriage – and one sure way of removing them all to allow any woman to successful carry to full term.

Target 1
Low progesterone
Progesterone is required for successful implantation and must remain at an elevated level to ensure that parturition does not prematurely – a decrease in progesterone is the natural trigger for labor. Inflammation involves the generation of the TNF alpha by the white cells, which reduces progesterone leading to re-absorption in early pregnancy and miscarriage and premature birth.

Elevated levels of insulin, resulting from insulin resistance (itself caused by inflammation), also reduce the level of available progesterone.

Target 2
Placental inflammation
Chronic inflammation is caused by chronic immune activation. The strength of the immune response can be increased by ‘complement activation’. TNF alpha can manufacture C5a (part of the ‘complement cascade) which one researcher called, ‘the key mediator in fetal injury.’

The immune system is design to hunt down and kill ‘non-self’, a fetus is partially ‘non-self’ (as it is derived, at least in part, from the father). To allow the fetus to grow in safety, the immune system switches from a state known as Th1 to Th2 (a state reserved for wound healing and pregnancy). Constant immune activation reverses this leaving the fetus at the mercy of the Th1 type immunity.

Target 3
Increased blood viscosity
In a wonderfully complex and orchestrated manner, detailed in A New Dawn, C5a attracts more white cells and thus more TNF alpha and free oxidizing radicals (FOR), this eventually leads to hypoxia. The immune response also damages the lining of blood vessels, the endothelium, generating platelet-activating factor (PAF) which is strongly pro-thrombotic. Both hypoxia and thrombosis result in growth restriction (hypoxia also promotes the generation of more PAF from the endothelial cells).

55 percent of all miscarriages are thought to be caused by increased blood viscosity.

Target 4
Endothelial micro-particles
Damaged endothelial cells give off micro-particles – these are pro-inflammatory, i.e. they attract further white cells, and pro-thrombotic. Micro-particles can easily intensify and prolong the immune response leading to miscarriage.

With four potential targets this may seem like a recipe for an entire pharmacopoeia but nothing could be further from the truth. A New Dawn details the response and shows how they are the result of persistent immune activation, perhaps more importantly it also shows how the cause of persistent immune activation can be detected and removed.

The chapter on miscarriage ends by saying, ‘supposed failure to conceive and recurrent miscarriage are devastating. But they HAVE NO REASON TO EXIST. Despite the trauma involved and the seeming multiple threats to the embryo, the situation is very simple. Persistent immune activation is the common theme that links these disparate pathologies. In Chapter 6 (of A New Dawn) you will find the means of preventing such activation. Should you choose to take advantage of this knowledge you can look forward to a massively increase chance of delivering as many healthy babies as you desire.’

As a society we have become conditioned to expect solutions to come in a child-proof screw-capped bottle provided by our MD. As Dr Quenby rightly observes, ‘so many women feel doctors are brushing them off because they say there is nothing they can do’ but now the answer lies in your own hands – not by taking Prenisalone and playing Russian roulette with chickenpox but by understanding your own body. You do not need the sanction of your MD, just the willpower to discover what they refuse to see. Dr Quenby’s work is a false dawn but one that will grab the headlines now and in another three months when it reappears in a clutch of women’s magazines, by then, you could be happily and safely pregnant. Good luck.


Following the Human Reproduction and Embryology
conference in Copenhagen (June, 2005) there has been huge
interest in the claim, made at the conference, that a commonly
used steroid could solve the problem of miscarriage,
particularly recurrent miscarriage that effects as many as 3
percent of US women of childbearing age.
It is generally agreed that between 50 and 70 percent of
conceptions fail but the use of a steroid that, according to the
State of California Environmental Protection Agency, is known
‘to cause cancer or reproductive toxicity’, is not the answer.
Prednisalone, the steroid in question, is also known to
contribute to congestive heart failure, hypertension and latent
diabetes and can leave adult users at risk of death from
chickenpox and measles that, through a propensity to mix with
young mothers and their children, they are very likely to come
into contact with.
The researchers concerned (a team from Liverpool University
in the UK) are quoted as saying, ‘an overreaction of the
immune system may lead a woman’s body to attack a
developing embryo and thus terminate the pregnancy.’