Learning from the experts

Thanks, Malcolm! We will probably defer the donor. I had the same explanation in mind but my colleagues were telling me that it's a group O donor while I thought it's a weak subgroup of A with anti-A1.

Essentially, this is because the A1 antigen is qualitatively different from any other A antigen.  As a consequence, all individuals with an A subgroup of any kind are capable of producing an anti-A1, which would explain the reaction with A1 cells, but not A2 cells.  In addition, the different A types, including, in this case, A1, are, in effect, a continuum from the strongest A1, right down to the weakest, for example, Am, and, in some cases it is impossible to detect any A antigen on the red cells, but it is possible to detect A substance in, for example, saliva, which would explain the results of the adsorption/elution testing.
I really would advise against ABO genotyping, unless you are really interested (and I wouldn't blame you if you were), as it is a very expensive technique which won't tell you in which "pool" to put the donor (A or O).  This will still be subjective.
If it is just that you are concerned that this patient could be "dangerous", in theory they probably could be (although, in practice, probably not so) and I would enthusiastically thank the donor for giving, but with an explanation detailed enough to let them know why (not over-burdening them with science, while also not treating them as an idiot), ask them not to donate again in future.

Thank you, guys, for explaining. 

Thank you, guys, for explaining. 

Because of the normal B antigens on the cells, so we can see strong reaction on MF with anti-AB.

Be aware that most Anti AB these days is a blend of anti A and Anti B monoclonal and is not strictly an anti AB.

Don't forget, also, that an individual who is AB has the A and B antigens on each and every erythrocyte.  The antigens themselves are NOT direct gene product, as they are, in effect, immunodominant sugar residues, and only proteins can be direct gene products.  In the case of the A and B genes, the direct gene products are, respectively, N-acetyl-D-galactosaminyl transferase and D-galacosyl transferase, both of which transfer their respective sugars from a UDP donor molecule.  However, these two enzymes are competitive.  As a result, sometimes the A transferase "wins the battle" between the two, and the A antigen ends up being expressed more strongly on the red cells than the B antigen, and sometimes the B transferase "wins the battle" between the two, and the B antigen ends up being expressed more strongly on the red cells than the A antigen.
In the case of the latter, an individual who is genetically A2B can, phenotypically, appear to be A3B, and so genotyping the individual may not help.  All that having been said, the fact that (roughly speaking) 50% of the antigens expressed on each red cell will be a normal B antigen, it is not surprising that there would be no"mixed-field" reaction with anti-A,B.

I was thinking about a 5 screen panel by SIAT or GEL. If everything reactive I will set up some cord and group A and B cells .
 

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