And no it does not.
Anti-D is ‘all about the next baby’.
In this blog post, I explain why that is.
Much of the information in this blog post is taken from my forthcoming book, Anti-D explained. More on that below.
Meet the antigens
First, it’s important to know what an antigen is. An antigen is a substance that is foreign to the body. When an antigen is detected by your body, your body mounts an immune response to it. In simple terms, your cell plasma cells start to generate antibodies to counteract the antigen. This is called a primary immune response. It leads to the production of antibodies, which we call immunoglobulin M, or IgM antibodies.
Once these IgM antibodies have counteracted the offending antigen, the body stops producing them. Cleverly, though, your body retains a memory of how it needs to respond if it encounters the same antigen again. That’s only sensible and it’s a mechanism which stops us from passing the same cold around forever. Once somebody has developed antibodies to a particular antigen, if the same antigen does enter the body again, the body mounts what is known as a secondary immune response. This occurs much faster than a primary immune response. Even more importantly for our purposes, the antibodies that it produces will come in a slightly different form. This time, they are called immunoglobulin G or IgG.*
* Yes, I know it’s a bit more complex than this if you dig into the science. Don’t write in. I’m not writing this for a PhD in immunology. I’m writing it because I explain this stuff to lay people and busy professionals who need the basics.
A primary response is what can happen if a rhesus negative woman encounters rhesus positive blood and her body responds to it by creating antibodies.
What would happen naturally?
Let’s pretend for a moment that we don’t have any injectable Anti-D (Rhogam®). What would happen ‘naturally’? Well, the woman’s body will recognise the anti-D as foreign. When that happens, it will mount a primary immune response. She would make IgM antibodies to the rhesus positive cells. Once the rhesus positive blood cells have all been cleared from her bloodstream, her antibody production will slow down and then stop. But her body will retain the memory of how to create them.
And now we now have a problem.
Because if she becomes pregnant with another rhesus positive baby in the future, her body now has a ‘template’ to make IgG antibodies against the baby’s blood. This can cause problems for a later rhesus positive baby. It won’t affect a later baby who is rhesus negative.
All of this explains why women are offered an injection of Anti-D in various situations. The manufactured version (actually a medicine made from blood) ‘clears’ any antigens that a pregnant woman may encounter if her rhesus positive baby’s blood enters her bloodstream. The manufactured Anti-D prevents the need for the woman’s body to make natural anti-D antibodies. And that means that future babies are not at risk from those antibodies.
Why antibody size matters
A hugely important thing to know at this point is this: IgM antibodies are about six times as big as IgG ones.
IgG antibodies can cross the placenta. IgM antibodies can’t.
So a woman who is mounting a primary immune response to rhesus positive blood cells is not going to be producing the type of antibody that can cross the placenta to harm her growing baby.
But a woman who is mounting a secondary immune response will produce the far smaller IgG antibodies. Those can cross the placenta.
During the primary immune response which involves the big IgM antibodies, the baby in utero is not at risk.
Why timing is key
But the difference between the primary and secondary immune responses is only one part of the answer to this question.
Another element of this is the timeframe of the process of antibody production. Which varies, depending on the antibodies.
Some antibodies can be produced within days. But the primary immune response to the rhesus factor can take up to six months. The rhesus factor isn’t produced in a baby’s blood until near or during the second trimester of pregnancy. And it can take up to six months for the primary immune response to stop.
Don’t forget that the primary immune response doesn’t pose a threat to the current baby because IgM is too big to cross the placenta.
By the time all of these timeframes have been added together, there’s not much chance of that same baby encountering IgG through a secondary immune response. He or she has almost certainly been born before that happens. Future siblings may encounter problems if they are rhesus positive, though. That’s because now their mother has a template for creating IgG antibodies that are small enough to cross the placenta into the baby’s bloodstream.
But Does antenatal Anti-D help the current baby?
Antenatal Anti-D is not about protecting the current baby.
Into the unknown
There is still a lot we don’t know in this area. We know that pregnant women have altered immune systems. This is so that their bodies do not reject their babies. Because at least half of a baby’s genetic material comes from someone else. Sometimes more, when assisted fertility methods are used. But we don’t know enough about how that works. We are beginning to form some theories about how the altered immunity of a pregnant woman might be related to some of the problems that pregnant women occasionally face. But there is much we don’t know about maternal and fetal immunity in general. And there are also big gaps in our knowledge about anti-D, sensitisation and related issues.
What don’t we know?
- As I said above, we know that IgG can cross the placenta. This is generally a good thing. It means that babies in utero gain immunity to things that their mother has already gained immunity to. But it’s not ideal in relation to the creation of anti-D. Given that nature generally gets it right most of the time, is there more that we don’t yet understand about this? Are there things that might affect a woman’s immune response to anti-D?
- When a woman decides to have manufactured Anti-D during pregnancy in order to possibly protect her future babies, this will enter the bloodstream of her current baby. We think that about ten per cent of it crosses the placenta. But we don’t know what effect/s this might have on that baby. It’s possible that it might have a different effect on rhesus positive and rhesus negative babies. We don’t know.
There are always more questions. For now, I hope that this has explained why manufactured Anti-D given routinely in pregnancy does not benefit the current baby. It may indeed benefit future ones and it is only one tiny element of a bigger picture.
Please also let me finish with a caveat: I am not an immunologist, and our understanding of this area is growing. There is much we don’t know, but things also change. Please always look carefully and critically at information you’re being offered.
For lots more information on Anti-D and related decision-making, see my book, Anti-D Explained. It has been written to explain the issues, answer key questions and share information about what we do and do not know about Anti-D. I look at the pros and cons of this from research evidence and current thinking. I help you understand the risks and benefits and explore what we can and cannot know. The aim is to help you to make the decision that’s right for you.
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