CD89, the human immunoglobulin A (IgA) Fc receptor (FcR), is a potential target for antibody-based therapeutics, but little is known about its expression and modulation in vivo. In this study, we examined the expression pattern of CD89 and its signalling subunit, the FcR g chain, on circulating myeloid cells and in various tissues. Our results showed a wide tissue distribution of CD89 þ cells. Thus, CD89 þ cells were evident as clusters in tonsils and appendix and scattered in varying numbers in lymph nodes, kidney, liver, intestinal mucosa, bronchoalveolar lavage and peritoneal fluid. Most CD89 þ cells were identified as neutrophils with high levels of CD89. A few recently emigrated macrophages (CD14 low ), weakly positive for CD89, were occasionally found in the tissues and more often in the peritoneal fluid. The level of CD89 on neutrophils in tissues and peripheral blood was similar, whereas on monocytes it was much lower in the tissues than in blood, and it was absent on CD14 -/CD68 þ intestinal lamina propria macrophages. Conversely, we detected much higher levels of the FcR g chain in monocytes than in neutrophils, but the FcR g chain was also downregulated in tissue macrophages as well as in in vitro-differentiated monocytederived macrophages and dendritic cells. The implications of our current findings on the biological functioning of CD89 are discussed.

We tested the hypothesis that swabs from the nasopharynx carry a higher viral load than swabs from the oropharynx in patients with real-time polymerase chain reaction (PCR)-confirmed influenza infection. Using flocked swabs, oropharyngeal and nasopharyngeal samples were harvested from hospital-admitted influenza patients no later than 3 days after the initial detection of influenza virus. Comparison of cycle threshold (CT) values was performed to assess differences in viral load in the specimens. Seventeen patients were diagnosed with influenza B, 14 patients with influenza A(H1N1)pdm09, and one patient with influenza A(H3N2). Nasopharyngeal samples were positive at a lower CT value than the oropharyngeal samples [mean difference in CT 5.75, 95 % confidence interval (CI) 3.8-7.7, p < 0.01], suggesting that, on average, the calculated viral load of the nasopharyngeal samples was 54 times higher (95 % CI 13.7-210.8) than those of the oropharyngeal samples. The corresponding difference in the calculated viral load for influenza A(H1N1)pdm09 virus was 23 times (95 % CI 3.8-136.2, p < 0.01) and for influenza B virus, it was 80 times (95 % CI 9.3-694.6, p < 0.01). In patients with acute influenza, nasopharyngeal swabbing was clearly superior to oropharyngeal swabbing in terms of diagnostic yield by real-time PCR.