MHC molecule expression in laryngeal epithelium of patients with laryngopharyngeal reflux compared to normal subjects

Objectives. We recently demonstrated an increase in the MHC-associated molecule, β-2-microglobulin in laryngeal epithelium from patients with laryngopharyngeal reflux (LPR). This could not be accounted for by an increase in MHC Class I, particularly in the superficial layers where Class I is weakly expressed. We hypothesised that this reflected an increase in CD1d, a non-classical MHC molecule. Methods. Posterior laryngeal biopsies were obtained from 10 controls and 11 LPR patients. Multicolour immunofluorescence microscopy was used to measure expression of CD1d, CD161 (NK/NKT marker), CD4/8 T-cells, macrophage, neutrophil and eosinophil antigens. Two-way analysis of variance and unpaired T-tests were performed on transformed data. Results. Expression of CD1d increased from basal to superficial layers, and was marginally raised in LPR (P = 0.067), whilst CD161 increased significantly (P = 0.02). While CD161(+) cells were distributed throughout the epithelium, CD8(+) T-cells were localised to the deep, MHC class I-expressing layers. EMBP was significantly reduced in LPR (P = 0.01). Conclusions. CD1d and MHC class I exhibit reciprocal expression patterns, which are reflected by the distribution of cells expressing their respective ligands (NKT cells and CD8(+) T-cells). An increase in CD1d in LPR may be responsible for the increase in β-2-microglobulin observed, and is associated with a significant increase in NKT-cells. The CD1d-NKT cell axis may be a crucial part of maintaining tolerance in the laryngeal mucosa and changes in this system may be responsible for the persistence of inflammation in LPR.