monopolova

I've seen it at least 2, maybe 3 times where reactions were consistent (ie repeatable) but didn't behave as expected - first of all, generally weak reactions, nothing stronger than a strong 1+ in gel, but reacted with some (not all) homozygous Jka cells and some (not all) cells that were heterozygous. each time, we threw more cells at it to prove/disprove the anti-Jka conclusion and each time the only consistency was that all of the reactive cells had the Jka antigen. could it have been some other antibody for which our panel cells didn't note the corresponding antigen? sure. but i wouldn't ignore the consistent presence of the Jka antigen on the reactive cells...

I should have also said that there is an excellent Blood Group Review available, viz Hamilton JR.  An update to Kidd blood group system.  Immunohematology 2024; 40: 28-33.  DOI:  10.2478/immunohematology-2024-005.

I worked in Red Cell Immunohaematology for most of my 43 years before retirement, including two times at the International Blood Group Reference Laboratory (IBGRL), and for over a decade at one of the NHS Blood and Transplant Centres in London.  During that time, I saw some pretty weird Kidd antibodies, but never came across an example of one that reacted with red cells with Jk(a) heterozygous expression, but not with Jk(a) homozygous expression.
One such "weird" type (although I never saw one) was the extremely rare, dominant inhibitor type In(Jk), similar, but, of course, not identical to In(Lu).  These red cells usually type as Jk(a-b-), but their true Kidd type can be ascertained by Adsorption and elution tests..  These red cells are also more resistant to haemolysis by 2M Urea than red cells with "normal" expression of the Kidd antigens, but less resistant to haemolysis by 2M Urea than true "amorphic" Jk(a-b-) red cells.
There are approximately 14, 000 copies of the Kidd carrier molecule per red cell (quite a small number, when compared with some other carrier molecules, such as the D antigen).
The amino acid residue that defines either the Jka or Jkb antigens is very close to the red cell membrane in the 4th extracellular loop but is largely “hidden” by the 3rd extracellular loop (steric hindrance).
 Both facts may contribute to the weak reactions between Kidd antibodies and Kidd antigens.

Schematic of the Kidd carrier molecule (after Wester ES, Storry JR, Olsson ML.  Characterization of Jk(a+weak): a new blood group phenotype associated with an altered JK*01 allele.  Transfusion 2011; 15: 380-392.  DOI: 10.1111/j.1537-2995.2010.02795.x.
In this paper, Wester et al also describe weakened forms of both the Jka and the Jkb antigens, but in each case, the amino acid substitution is remote from position 280 of the mature protein. 
 In addition, an individual with the Trp171Arg mutation with weak Jk(a) expression has produced an anti-Jk3 or anti-Jk3-like antibody, and so they may be “dangerous patients” (Whorley T, Vage S, Kosanka J, Lose SR, Sandquist AR, Copeland TR, Westhoff CM.  JK alleles associated with altered Kidd antigen expression.  Transfusion 2009; 41 (Suppl.): 48A-49A (abstract).
Lastly (for now anyway!), most foetal red cells sensitised by maternal antibodies react only with anti-IgG, but I (and a colleague Grant Webb) have both noticed, but not published, occasions when such red cells also react with anti-C3d and, in one case, only anti-C3d (see genuine photographs below)..

Yes. And worse, some cells react differently, including having no reactivity,  as compared with cells of the same degree of zygosity.  Thus the possibility of Kidd antibodies needs to be seriously considered when the recipient is negative for one or both antigens and the panel is reactive but without clearcut specificity for Jka or Jkb.

Hello all,
If you had a patient who appeared to have anti-D and anti-C and titers between the two were quite discrepant, is that sufficient evidence to effectively confirm anti-D?  This assumes that anti-G, if present, would react with cells containing the C or D (and G) antigens with similar titer (which I do not know to be true, but perhaps someone on here does know this).  Perhaps the G antigen is represented in different quantities on RhD vs C antigen bearing cells ....
Thank you! 

Hello all,
Any differences between Ortho Panel A versus Ortho Panel B which would argue that a CLS should favor (from a serology perspective) using Panel A first to work up an antibody ID (as opposed to using Panel B first)?  I imagine that if you statistically rule out your antibodies using either Panel, you should be good.  But, perhaps there is a nuance I am missing.
Thanks!

To be honest, I don't know, BUT, given that it would be almost impossible to know whether the donor of the red cells is a single dose En(a+), as it is with most of the 901 Blood Group Series antigens, I would have thought that any donor with a normal MNS phenotype would do, but that the pregnancy should be monitored by MCA Doppler.