The identified KEL mutations of the two probands are novel and inherited. The antigen absent from the red blood cells (RBCs) of Probands 1 and 2 are named KALT and KTIM, respectively. KALT is unique in that it is the only Kell antigen sensitive to treatment of RBCs by trypsin.

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This case demonstrates the potential immunosuppressive properties of RhIG for down regulation of a possible clinically significant alloantibody, not anti-D, where no D+ antigen is in the circulation of the mother. The case illustrates the potential utility for using RhIG to modulate antibody levels in situations other than for classical suppression of anti-D production. Although the mechanism in this case is unknown, TGFβ-1-mediated or antibody-mediated immunosuppression to soluble nonparticulate antigens are possible mechanisms.

BACKGROUND: RBCs of the Hy– phenotype have, in the past, been typed as Gy(a+w), Hy–, Jo(a–), and RBCs with the Jo(a–) phenotype type Gy(a+), Hy+w, and Jo(a–). Anti‐Hy and anti‐Joa are difficult to identify mainly because appropriate reagent RBCs are poorly characterized. Historically, anti‐Joa has not reacted with RBCs with either phenotype. This report describes a case of an anti‐Joa that shows Hy– RBCs express some Joa antigen, albeit weakly. CASE REPORT: Anti‐Joa was identified in a serum sample of a 71‐year‐old woman. The antibody reacted 1+ to 2+ by the IAT with all untreated and ficin‐treated panel RBCs and did not react with Gy(a–) RBCs and Jo(a–) RBCs. Unexpectedly, the serum sample reacted weakly with six of eight RBC samples with the Hy– phenotype. The anti‐Joa was adsorbed onto and eluted from Hy– RBCs, indicating the presence of weak Joa antigen. The patient's RBCs typed Gy(a+), Hy+, Jo(a–). DNA studies using PCR‐RFLP analysis showed the patient to be homozygous for the JO allele, which is consistent with the serologically determined Jo(a–) status. CONCLUSION: The DNA and serologic evidence of this case show that Hy– RBCs may express low levels of Joa antigen, which contradicts previously published data concerning the Joa type of Hy– RBCs.

This case is an additional example of a chloramphenicol-dependent antibody. It demonstrates how the laboratory investigation of drug-related phenomena is dependent on testing the drug from that reacts in vivo.