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M antigen and antibody


MinerJ

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Hi All,

First time posting so not sure if this is the right place for this general enquiry.

I have read in different literature about anti-M antibody and its class, but none seem to agree with one another. Some say that anti-M antibody is mainly IgM class, others that it is primarily IgG, and others mention that it is even. So anyone knows what the real answer is?

Also, I have read that anti-M IgG class is capable of direct agglutination. I am aware that the M antigen is a high-frequency antigen on the red cell, but how would this resolve the issue which IgG class have in spanning across the zeta potential of the red cell to cause agglutination?

And if someone can explain to me how this sometimes causes discrepancy in the reverse group, I will also be grateful

(I apologise for my lack of knowledge, just starting my specialist)

Regards,

Jermin 

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First of all, welcome to this marvellous site, and NEVER, EVER apologise for a lack of knowledge; we all had to start somewhere!

Almost all, but not absolutely all, samples of anti-M contain an element of IgM, whilst about 78% contain an element of IgG.  A small percentage of these will, in effect, be only IgG.

Be a bit careful of your terminology.  It is true that the molecule upon which the M antigen is located (glycophorin A) is amongst the most abundant protein found on the red cell membrane, but both M and its allelomorph (or antithetical antigen) N are both polymorphic, rather than high prevalence.

The amino acids that form the M antigen are at the extreme external end of the glycophorin A molecule, which makes them available to the antibody.  So, the M antigen can be present in abundance and are readily sensitised.

IgG anti-M (and anti-N, come to that), are not unique in causing agglutination without a potentiator; IgG ABO antibodies can also do this.  If you have a cord sample from a baby suffering from ABO HDN, and it is stored in the fridge over night, you can often see agglutination in the sample the following morning.  This cannot be an IgM ABO antibody formed in the baby, and so it must be a maternal antibody.  However, IgM antibodies cannot pass through the placenta, and so the ABO antibody present, causing the agglutination, must be a maternal ABO IgG antibody.

If the reverse grouping cells are M+, particularly if they are M+N-, and the patient's plasma contains an anti-M, this will cause agglutination.  SO, if the patient is group A, but the reverse grouping A1 cells also happen to be M+N-, the group A patient will appear to have an anti-A in his/her plasma.

I hope that helps a bit.

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Hi Malcolm,

Thank you for explaining it to me clearly, always look out for your replies in posts. It has been a great help, and I have already gained a lot of insight by going through the forum thanks to you and other contributors. I will ensure that I appreciate what little knowledge I do have a bit more in the future. 

Jermin

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1 hour ago, galvania said:

And just a practical tip.  Best way to detect most anti-M is in an IAT with incubation at 20°C rather than 37°C.  No references for this, just lots of practical experience

I wouldn't argue with that, IF you want to detect clinically insignificant examples of anti-M (i.e. the vast majority of them), but the ONLY way to detect clinically significant examples of anti-M is at 37oC.

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  • 3 weeks later...
On 20/08/2017 at 12:51 PM, Malcolm Needs said:

IgG anti-M (and anti-N, come to that), are not unique in causing agglutination without a potentiator; IgG ABO antibodies can also do this.  If you have a cord sample from a baby suffering from ABO HDN, and it is stored in the fridge over night, you can often see agglutination in the sample the following morning.  This cannot be an IgM ABO antibody formed in the baby, and so it must be a maternal antibody.  However, IgM antibodies cannot pass through the placenta, and so the ABO antibody present, causing the agglutination, must be a maternal ABO IgG antibody.

 

Decided to revisit the post, just because I was trying to find some information of ABO IgG antibody causing agglutination. I have yet to see any literature which mentions this, so I was hoping you, or anyone else, can explain to me how this is possible? Is it a similar situation like M antigen being present in the extreme end of glycophorin A? 

Bonus point for explaining it to me like I am a 5-year-old

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Okay, I'll try!

It is very unusual (although not unknown) for a baby to make either anti-A or anti-B at birth, as the immune system is generally too immature to produce such antibodies.  It is virtually unknown for a baby to make either an auto-anti-A or an auto-anti-B (it is incredibly rare for an adult to do this, let alone a baby), and a baby certainly will not produce any IgG antibodies.  If a baby is suffering from HDFN due to ABO, the antibody must, therefore, have been derived from the mother1.

For the mother's antibodies to transfer from her circulation to the foetal circulation, the antibody has to be IgG in structure (IgM will not cross the placenta).  So, if the baby is suffering from ABO HDN, the baby's red cells must be coated (sensitised) with maternal IgG ABO antibodies.  If the baby's sample is put at 4oC (put in a fridge) overnight, when it is examined the next morning, by tipping the sample, agglutination can be seen (usually macroscopically), and this can only be due to maternal ABO IgG antibodies.  In Addition, a paper by Voak et al2 spoke about anti-A IgG antibodies causing agglutination.

Is this because the ABO antigen is close to the end of the carrier molecule (like M is near the end of glycophorin A)?  Well, certainly the N-acetyl-D- galactose molecule that makes up the A antigen (and the D-galactose molecule that makes up the B antigen), is found at the end of the oligosaccharide molecule upon which the ABO antigens are found, but, in addition, there are some 250, 000 and 370, 000 A antigens expressed per  red cell (although there are some 800, 000 GPA sites per red cell3).  The site of the ABO antigens are, therefore, likely to be important.

References:

1.  Klein HG, Anstee DJ.  Mollison's Blood Transfusion in Clinical Medicine.  12th edition, 2014, Wiley Blackwell, chapters four and twelve.

2.  Voak D, Abu-Sin AY, Downie DM.  Observations on the thermal optimum, saline agglutinating activity and partial neutralization characteristics of IgG anti-A antibodies.  Vox Sanguinis 1973; 24: 246-257.  DOI 10.1111/j.1423-0410.1973.tb02636.x.

3.  Reid ME, Lomas-Francis C, Olsson ML.  The Blood Group Antigen FactsBook.  3rd edition, 2012, Academic Press, page 62.

I hope that helps, even if it doesn't win me the bonus points!!!!!!!!

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Yes, we use this kind of method to determine if there is ABO HDN present, putting the elution with reagent A,B,O cells respectively in the refrigerator( 4 degree C) overnight, then gently tip the tubes  to see the agglutination.

The O cells is as a negtive control, in case there are other cold antibodies interfere with the test.

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Anti-M does have both IgM and IgG components. It primarily reacts as IgM but can carry over to IgG. We had one last week. The IgM component caused an ABO discrepancy by reacting with with M+ A1 reverse cells in an A Pos patient. The IgG component showed up at coombs phase after the addition of Anti-IgG. We had to transfuse M neg units to have compatible cross matches.

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