Head and neck squamous cell carcinomas (HNSCC) are highly immune suppressive and aggressive malignancies. As part of the tumor microenvironment, exosomes contribute to this immune suppression. The Fc receptor CD16 is widely expressed on monocytes, neutrophils, and natural killer (NK) cells and is involved in antibody-dependent cell-mediated cytotoxicity (ADCC). Here, surface levels of CD16 on total exosomes and tumor-derived exosomes (TEX) from plasma of HNSCC patients were analyzed regarding their potential as liquid biomarkers for disease stage. Exosomes were isolated from plasma using mini size exclusion chromatography. TEX were enriched by immune affinity capture with CD44v3 antibodies. On-bead flow cytometry was used to measure CD16 levels on total exosomes and TEX. The results were correlated with clinicopathological parameters. Total exosomes from HNSCC patients had significantly higher CD16 levels compared to TEX. Further, CD16 surface levels of total exosomes, but not TEX, correlated with clinicopathological parameters. Patients with advanced tumor stages T3/4 and Union for International Cancer Control (UICC) stages III/IV had significantly higher CD16 levels on total exosomes compared to patients with early tumor stages T1/2 and UICC stages I/II, respectively. Overall, CD16 positive exosomes have the potential as liquid biomarkers for HNSCC tumor stage and aggressiveness.

Polymorphisms in the Fcγ-receptor (FcγR) have been associated with increased susceptibility to systemic lupus erythematosus (SLE). There is a paucity of data on FcγR expression pattern in pediatric subjects with SLE. The aim of the study was to assess the expression of various FcγRs by flow cytometry in children with pediatric-onset SLE (pSLE).
Thirty-one children aged 0-15 years fulfilling 2012 Systemic Lupus International Collaborating Clinics Classification Criteria for SLE were enrolled. Disease-active (n = 14) and the inactive group were delineated using the SLE Disease Activity Index (SLEDAI). Thirteen age- and sex-matched controls were also enrolled. Blood samples of cases and controls were assessed for CD64, CD32B and CD16 expression on B lymphocytes, neutrophils and monocytes by flow cytometry using standard techniques. Median fluorescence intensity (MFI) and percentage expression were calculated using the FACS DIVA software and Kaluza software.
Median fluorescence intensity and percentage expression of CD64 on monocytes (MFI: 1.71 vs 1.51, P = 0.86) and neutrophils (MFI: 0.42 vs 0.64, P = 0.3) were comparable between patients and controls. MFIs of CD16 expression on neutrophils (3.47 vs 11.4, P = 0.05) and monocytes (1.28 vs 3.45, P = 0.07) were lower in patients compared to controls. CD32B expression on lymphocytes (MFI: 0.56 vs 1.37; % expression:18.3% vs 12.32%) was also comparable between cases and controls. Expression of CD64, CD16, and CD32B were also comparable between patients with active and inactive disease.
No significant differences were observed in FcγR expression between patients and controls. However, the overall trends of FcγR expression and decreased CD16 on monocytes and neutrophils are in consonance with data from larger cohorts of adult SLE patients.
© 2018 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd.