Transporter associated with antigen processing deficiency: an additional condition associated with bronchiectasis.

摘要

We read with interest the review on bronchiectasis by King et al. It is an authoritative synthesis of our current knowledge of this entity. Therefore, we do not intend to criticize this article, but want to complete it by adding transporter associated with antigen processing (TAP) deficiency to the list of conditions associated with bron-chiectasis. TAP is composed of a TAP1 and a TAP2 subunit inserted in the membrane of the endoplasmic reticulum (ER). It translocates peptides derived from the degradation of endogenous proteins into the lumen of the ER, where they are loaded onto newly synthesized human leucocyte antigen (HLA) class I molecules stabilized by peptide acquisition and migrating to the cell surface to present peptides to CD8~+ T cells. Without a functional TAP, most HLA class I molecules remain peptide free and unstable, so that their cell surface expression is severely reduced (30-fold to 100-fold compared with normal cells).