I recently heard from my teacher that a recent discovery shows that blood group antibodies are created in response to some bacteria that infect the baby in the first few month after parturition and that the cell coats of these bacteria resemble the respective blood antigen. If that is so how does maternal-foetal ABO incompatibility occur? What about the belief of genetic inheritance of the blood group, won't it then depend on the type of bacteria infecting the child? Another major point of doubt i have is that the newborn won't have a very active immune system, and gets most of its immunity from the mother right? so how does it develop the antibodies against the bacteria?
Blood grouping antibodies caused by bacteria
- Thread starter sw2kool
- Start date
- Joined
- Apr 18, 2012
- Messages
- 577
- Reaction score
- 698
oh crap! the surface antigen is the source of the specificity right?
- Joined
- Jan 29, 2010
- Messages
- 1,001
- Reaction score
- 64
Rh incompatibility is a different case. i'm not talking about that. i'm asking about hdn due to abo blood grouping.
Last edited:
- Joined
- May 19, 2006
- Messages
- 384
- Reaction score
- 4
Mm, as far as I've heard, there's no solid answer on your question yet. It's all theory atm because we don't know exactly how we develop ab against other blood types with no exposure to it.
The bacteria is just one theory. It doesn't explain the ABO incompatibility while it's still a fetus as you pointed out above.
I would also say that babies aren't like SCID patients. They do have some immunity, innate and acquired - otherwise vaccines wouldn't work. So they can fight off some things - colds, bacteria, etc, but they don't have as good of an immune system as a young adult, hence needing mother's milk/ab.
The bacteria is just one theory. It doesn't explain the ABO incompatibility while it's still a fetus as you pointed out above.
I would also say that babies aren't like SCID patients. They do have some immunity, innate and acquired - otherwise vaccines wouldn't work. So they can fight off some things - colds, bacteria, etc, but they don't have as good of an immune system as a young adult, hence needing mother's milk/ab.
- Joined
- Jan 29, 2010
- Messages
- 1,001
- Reaction score
- 64
Oh, OK. Well I don't understand what you're confused about. It's the antibodies that allegedly develop due to bacterial cross-reactivity, not the blood antigens themselves.
The mother already has the antibodies. The IgG crosses the placenta, and reacts with the blood group antigens in the fetus.
I am really confused about what you're asking.
It happens when the mother is Type O, and IgG anti-A and anti-B antibodies are made. IgG2 passes placenta, thus hemolysis.
Yes, blood groups are genetic. Didn't you do Punnett squares in biology? ex: iAiA father, ii mother, all children i iA. Thus the mother is Type O and has a Type A fetus. Anti-A IgG2 crosses placenta and binds to A antigen of the fetus.
Last edited:
- Joined
- Jan 22, 2010
- Messages
- 4,920
- Reaction score
- 43
He's asking why, ex nihilo, people have anti-A and anti-B isohemagluttinins.
The current theory professed by my Canadian professor is that it helped to delineate the races of Cro-Magnons from Neanderthals.
/trollface
The current theory professed by my Canadian professor is that it helped to delineate the races of Cro-Magnons from Neanderthals.
/trollface
I know blood groups are genetic!! Look, according to what my teacher said recent study shows that blood antibodies develop because of bacterial infection imitating blood antigens post parturition. So my question was, how does that fit in with genetic blood grouping if the blood antibody developed is in response to a bacteria that infects the baby after birth.
- Joined
- Mar 6, 2011
- Messages
- 49
- Reaction score
- 24
The way I heard it in my blood banking course when I was a Medical Technology student was that these glycoproteins/glycolipids are present on the surface of ubiquitous bacteria, so it's not a one time infection that elicits anti-A or anti-B antibodies. Somewhere between birth and 1 year of age, infants start showing the appropriate ABO antibodies due to this exposure. As to why this constant exposure doesn't eventually result in anergy, I have no idea!
Also, a fun fact about the genes for the ABO blood groups: they code for an enzyme that links sugars to proteins/lipids and not the actual A/B antigens themselves.
- Joined
- Feb 17, 2009
- Messages
- 334
- Reaction score
- 3
HDFN due to ABO incompatibility occurs as a result of maternal antibodies (anti A,B) crossing the placenta and attacking the baby's red blood cells. The baby expresses A and B antigens on his/her red cells at birth (albeit weakly - which is why HDFN owing to ABO incompatibility is typically mild). The fact that the baby isn't expressing any ABO antibodies as of yet is immaterial.
People are thought to develop ABO antibodies as a result of some as-of-yet unidentified environmental exposure, perhaps bacterial antigens. SoDakMLS has a nice description above. This generally doesn't occur before 4 months of age. You produce antibodies against non-self - therefore, if you're group A, you won't make anti-A when you are exposed to A-like antigens on bacteria (your immune system is too smart for that), but you will make anti-B when you are exposed to B-like antigens on bacteria.
If you really want to hurt your brain, look up "acquired B antigen".
Last edited:
