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Posted: March 28, 2006

Addenda: Mar. 29 & 31, 2006; Sept. 17 & 20, 2007

 

Is it necessary to determine the specificity of HTLA antibodies?

A Reference Laboratory supervisor in a Rocky Mountain state reports that for the past ten or so years her laboratory has used an 'in-house' panel of "HTLA antigen negative" reagent red cells to help them determine (in many cases) the specificity of an HTLA antibody, rather then merely calling the antibody a "probable HTLA-like antibody". They 'make' this panel from red cells that they acquire from antibody identification panels, based on phenotype information provided by the manufacturers. Of late, they have noted that reagent red cell manufacturers are providing less 'extended phenotype information' with the red cell panels, so that her laboratory no longer has enough information to create the 'in-house' HTLA antigen negative panel. This has forced them to re-define their policy about trying to actually determine the specificity of an HTLA antibody. They wonder if they are no longer able to identify the specificity of an HTLA antibody, would colleagues think that it is sufficient to merely call the antibody "HTLA-like", and focus on ruling out the presence of additional (underlying) alloantibodies? In the absence of an HTLA antigen negative panel, how do others determine the specificity of the HTLA antibodies they detect, or does it even matter?


The following comments have been received.

ADDENDA Mar. 29, 2006

  1. Professor W. John Judd at the University of Michigan Medical Center (attribution used with permission), reports that in his experience the term "HTLA" is a misnomer, usually applied to antibodies to KNOPS antigens, but some would consider Ch/Rg, Yta, Csa, JMH and LU antibodies to be part of that group. He reminds us that KNOPS antibodies are not always of high titer, and avidity has nothing to do with their weak reactivity; rather, it is a matter of low antigen site density on RBCs.

    Professor Judd says, "We try and identify the aforementioned specificities to the greatest extent possible, based on the reactions of ficin-treated RBCs and DTT-treated RBCs, serum inhibition and titration studies, and the results of antiglobulin tests with a monoclonal anti-IgG that does not react with IgG4. Antibodies to Ch/Rg and JMH do not react with ficin treated RBCs; anti-Ch/Rg are inhibited by pooled plasma; anti-JMH is nonreactive with DTT-treated RBCs and most examples do not react in antiglobulin tests with the monoclonal anti-IgG. Antibodies to Kna and Yta react variably with ficin-treated RBCs and are usually nonreactive with DTT-treated RBCs; sometimes it is helpful titrate the antibody against ficin-treated, DTT-treated