The loss of the CD16 B73.1/Leu11c epitope occurring in some primary immunodeficiency diseases is not associated with the FcgammaRIIIa-48L/R/H polymorphism.

Abstract

The loss of the CD16a, Fc receptor for IgG type III, (FcgammaRIIIa) B73.1/Leu11c binding epitope, detected by the monoclonal antibody (mAb) used in routine enumeration of NK cells or monocytes, has been observed in children with recurrent viral infections. It has also been linked with the change of leucine (L) to histidine (H) or arginine (R) at amino acid position 48 (FcgammaRIIIa-48L/R/H) in the CD16a receptor. The reactivity of the anti-CD16a clone B73.1/Leu11c mAb with monocytes and NK cells was examined in patients with primary immunodeficiencies (n=167), gastrointestinal malignancies (n=91) and healthy subjects (n=88). Cells of only 12 children, 11 with diagnosed primary immunodeficiency and one with recurrent bacterial infections were not reactive with B73.1/Leu11c mAb. In contrast to previous findings, no linkage between the loss of B73.1/Leu11c binding epitope and herpes virus infections was observed. Furthermore, the sequence analysis of the FcgammaRIIIa gene performed in these 12 patients and 11 healthy subjects revealed that all of them had FcgammaRIIIa-48L/L genotype. Thus, the loss of B73.1/Leu11c binding epitope was not associated with the FcgammaRIIIa-48 polymorphism. The commonly described FcgammaRIIIa-158 polymorphism was determined to be 158V/V in 11 patients and 5 healthy subjects. Moreover, no linkage between FcgammaRIIIa-48L/L and -158F/F genotypes was observed. It is suggested that the loss of the B73.1/Leu11c binding epitope is connected with primary immunodeficiency disorders, but not associated with the FcgammaRIIIa-48 polymorphism.