ABO System: The Sesitizing Event

[rravkin@aol.com]

Dear Subscribers,

I present this thread with some hesitation as I am not sure of it's practicle value, but I do believe it will lead to some greater understanding of Antibodies and their production through the humeral response.

We have O individuals that produce Anti- A,B IgG class antibodies. We have A and B individuals that produce Anti- B and Anti- A respectively that are IgM class antibodies. The question is, What is the sensitizing event that caused the respondent production of these antibodies, and when and where did it occur? Furthermore, because the O mother produces the Anti-A,B IgG class antibodies that will cross the placent; what kind of assistance, if any, does it offer the newborn in terestial survival given the idea that from a global perspective O type individuals are of the most survived humans on earth? Additionally, why is it that the A and B individual immune systems stop with the production of the corresponding IgM class antibodies, which will not cross the placenta? Are the production of these antibodies accomplished by the immune system via regular humoral response or are they genetically predetermined and produced phenotypically like normal cellular proteins and then released into circulation.

I appologize in advance if this thread is percieved as being missmatched for this site but I have a burning curiousity about this subject and I thought it would make for a fantastic topic of discussion because the ABO system is the basics for Blood Bank practice and it seems that the origin of the corresponding antibodies produced are not well understood. :)

[David Saikin]

The A,B,O antigens are ubiqutious in nature. They are all around and your immune system samples them from the time of your first breath. Hence Nature is the sensitizing event, they are naturally occurring. The shift to IgG (and this DOES NOT stop the production of the IgM versions) probably occurs when/if the fetus's rbcs encounter the mother's immune system . . .not all group O mothers have the IgG version. IgG is actively transported across the placenta - the specificity of the antibody is meaningless to this process. This is nature's way of providing immunity until the newborn's own immune system kicks in. I believe this process is well understood.

[rravkin@aol.com]

The A,B,O antigens are ubiqutious in nature. They are all around and your immune system samples them from the time of your first breath. Hence Nature is the sensitizing event, they are naturally occurring. The shift to IgG (and this DOES NOT stop the production of the IgM versions) probably occurs when/if the fetus's rbcs encounter the mother's immune system . . .not all group O mothers have the IgG version. IgG is actively transported across the placenta - the specificity of the antibody is meaningless to this process. This is nature's way of providing immunity until the newborn's own immune system kicks in. I believe this process is well understood.

David,

I greatly appreciate your response. What is it about the encounter with the mother's immune system that causes the shift to IgG production in the fetus? Asked another way; what is it about the encounter with maternal IgG that causes the production of IgG in the neonate? You also say that the sensitivity of the IgG that crosses the placenta is meaningless and yet this very IgG is what confers immunity for the neonate in the first three months of life. Do you mean that the aquired maternal IgG has broad specificity? When I referenced the AABB Technical Manual 15th Ed, The ABO System, it stated that O type persons produced anti A,B IgG class antibodies while A and B persons produced anti-B and anti-A respectively of IgM class. I was wondering why it is that the O type produce an IgG class while the A and B immune systems did not; because one could then speculate that an A or B mother would not pass their corresponding antibodies to the fetus if they were IgM class and, therefore, further speculate that the newborn would not have the same immune protection of that of one born of an O mother.

From your statement about the ubiquitious nature of ABO antigens one could speculate that production in the noenate of corresponding antibodies does not occur as a defensive process like that of alloantibodies but rather as more of an initial filing system, perhaps, on part of the noenates immune system. I will read up on this some more and I do appreciate any further responses.

[Malcolm Needs ☆]

Hi rravkin,

Jill Storry and Martin Olsson have comparatively recently published a fantastic review in Immunohematology.

Storry JR, Olsson ML. The ABO blood group system revisited: a review and update. Immunohematology 2009; 25: 48-59.

Some of this may go towards answering part of your questions, and I have taken the liberty of attaching most of the section from this review entitled, "Antibodies in the System". A further section, entitled, "Clinical Significance" goes on to discuss other aspects of ABO antibodies.

The whole review really is worth a read.

Best wishes,

Malcolm

:D:D:D:D:D

Storry JR.doc

[rravkin@aol.com]

Hi rravkin,

Jill Storry and Martin Olsson have comparatively recently published a fantastic review in Immunohematology.

Storry JR, Olsson ML. The ABO blood group system revisited: a review and update. Immunohematology 2009; 25: 48-59.

Some of this may go towards answering part of your questions, and I have taken the liberty of attaching most of the section from this review entitled, "Antibodies in the System". A further section, entitled, "Clinical Significance" goes on to discuss other aspects of ABO antibodies.

The whole review really is worth a read.

Best wishes,

Malcolm

:D:D:D:D:D

Thank you Malcolm; I was beginning to think that you weren't going to get involved with this thread. I have actually writen this book title down from a previous post. I will enjoy reading about this subject.

Thank you again.

Rravkin:)

[Malcolm Needs ☆]

Thank you Malcolm; I was beginning to think that you weren't going to get involved with this thread. I have actually writen this book title down from a previous post. I will enjoy reading about this subject.

Thank you again.

Rravkin:)

No, just been extremely busy for the last couple of days!

:)

[Fluffy agglutinates]

What is it about the encounter with the mother's immune system that causes the shift to IgG production in the fetus? Asked another way; what is it about the encounter with maternal IgG that causes the production of IgG in the neonate? You also say that the sensitivity of the IgG that crosses the placenta is meaningless and yet this very IgG is what confers immunity for the neonate in the first three months of life. Do you mean that the aquired maternal IgG has broad specificity?

If I may I think you are a little confused over what is actually happening at this stage of life...

Any IgG molecule will be transported by the placenta regardless of its specificity. This is what conveys protection in the first few months of life (i.e. the baby has the mother's immunity for a time).

Maternal IgG in the fetus does not cause production of IgG in the neonate. All Ig levels in newborns are low with the exception of IgG (but this is maternally derived). The acquired IgG specificities will depend on what the mother has produced.

After 18 months the IgG level will only be ~60% of an expected adult level.

I would advise trying an immunology book for further details (e.g. Roitt's Essential Immunology).

Hope this helps a bit!

[rravkin@aol.com]

Fluffy Agglutinates,

Thank you for your response. I do have an immunology book, Kurby Immunology, and I have some backround in it's study. I am aware that there is a broad spectrum of maternal IgG that crosses the placenta conveying immunity to the newborn. I unfortunately read what appear to be some general statements in the AABB Technical Manual 15th Ed. that prompted my thread. I was focused on the effect, if any, of materal IgG of the A B concentration because of what I read. Appearently, according to the article the Malcolm has suggested, the iniation of Anti A or B in the neonate is initiated do to the immune system's recognition of foreign proteins on the normal intestinal flora. These protiens are similar in structure to the A and B antigens.

Thank you again.