An autoanti‐Kp^b immunoglobulin M that simulates antigen suppression

Abstract

In antigen loss, antibody masking is excluded by a negative DAT. However, because typical DAT reagent does not detect IgM, such reasoning was inaccurate in the current case. In addition, an anti-Kp(b) resulted in RBCs typing k-, even though no anti-k was detected. Overall, this case suggests that an IgM may mask adjacent epitopes and illustrates the potential to mistake a non-IgG autoantibody as antigen loss.

A novel role for C3 in antibody-induced red blood cell clearance and antigen modulation

“…Similar findings have also been described in humans, with hemolysis of a subset of Kell RBCs yet antigen modulation of surviving Kell RBCs. [14][15][16][17][18][19][20] Thus, the RBC clearance, RBC survival, and antigen modulation observed in our murine studies parallel what is known to occur in humans. The current model is the first described in which C3 is involved not only in antibody-induced incompatible RBC clearance but also in apparent antigen modulation.…”

“…13 The phenomenology of antigen modulation in humans has been repeatedly described in the context of antibodies binding red blood cells (RBCs). [14][15][16][17][18][19][20] This outcome has been termed depressed antigen, antigen suppression, weakened antigenicity, and antigen loss and has been observed for multiple blood group antigens, including Kell, RhD, RhC, Rhe, Jka, Jkb, Gerbich, LW, AnWJ, and Cromer. Among these, antigen modulation has been described most frequently for antigens in the Kell system.…”

Transfusion of murine red blood cells expressing the human KEL glycoprotein induces clinically significant alloantibodies

“…We have previously reported RBC populations resistant to hemolysis in the hGPA system . In addition, KEL antigens are known to have the potential to undergo weakened antigenicity during incompatibility in human settings; ongoing studies are investigating clearance as well as clearance resistance mechanisms in our model.…”

DNA-based methods in the immunohematology reference laboratory

“…One must consider that the serological problem may involve the inheritance of a null allele, an autoantibody with a particular specificity masking an autologous antigen [39], or a new variant. Knowing the patient’s ethnicity, their parental and sibling phenotypes, and having a good understanding of which blood group systems express variants, can provide clues to the interpretation of molecular results or suggest further investigation like gene sequencing.…”