Objective. Allelic TAP polymorphism has been linked to susceptibility to Reiter's syndrome and was suggested to influence disease phenotype in HLA-B27 positive patients with ankylosing spondylitis. In the present study, we examined whether the human TAP alleles functionally differ in their translocation specificity for HLA-B27-binding nonamers.
Metho&. TAP translocation of a panel of HLA-B27-binding peptides was measured with a labeled reporter peptide containing an N-linked glycosylation acceptor site in streptolysin 0-permeabilized cells with different TAP alleles.
ResuZts. The different human TAP alleles tested did not measurably differ in their peptide specificity.
Conclusion. The polymorphism of human TAP does not affect the translocated repertoire of HLA-B27 ligands and is therefore unlikely to play a decisive role in the development of HLA-B27-associated disease.
One of the major predisposing factors in ankylosing spondylitis (AS) and bacteria-induced reactive arthritis is the class I major histocompatibility complex (MHC) protein HLA-B27 (1). However, only a small minority of HLA-B27 positive individuals will develop disease. Additional modifying or susceptibility genes have therefore been purported to act in concert with HLA-B27. Since a function of HLA-B27 is to present ~