Purpose: To evaluate lower tear meniscus and corneal sub-basal nerve plexus in primary Sjögren's syndrome (pSS) and Sicca syndrome patients. Methods: Cross-sectional study of 116 patients with Sicca syndrome associated with pSS and not associated with Sjögren's syndrome (non-SS Sicca) and 20 normal control subjects. Tear meniscus height and area were measured using anterior segment optical coherence tomography; corneal sub-basal nerve plexus density, length, and tortuosity were evaluated using in vivo confocal microscopy. Data analysis was performed using IBM-SPSS Statistics 24.0. Results: Corneal sub-basal nerve plexus density and length were significantly lower, and tortuosity was significantly higher in pSS and non-SS Sicca groups than in normal control subjects (P < 0.001; P = 0.018, respectively). Corneal sub-basal nerve plexus presented a strong association with Schirmer test I and tear breakup time. Cutoff values of sub-basal nerve plexus density (36.5 nerve/mm2) and length (12.5 mm/mm2) presented 80.2% to 81.9% sensitivity and 85% specificity for detecting Sicca syndrome patients. No significant differences were found between the 3 groups regarding tear meniscus height and area. Conclusions: Corneal sub-basal nerve plexus in vivo confocal microscopy may be a useful tool in the assessment of dry eye disease in Sicca syndrome, complementing the information provided by the conventional modalities used in dry eye disease evaluation.

Nanotechnology enabled the development of materials and devices with great utility in different fields of medicine. By using engineered-based nano-devices and structures, human biological systems may be controlled and repaired at a molecular scale, ultimately leading to a biological benefit. In particular, in the field of glaucoma treatment, nanotechnology may, for example, enhance drug residence time on the ocular surface and ocular bioavailability, as well as improve surgical success by both optimizing postoperative scarring and providing a wider safety window. Further studies are still needed to entirely explain the pharmacodynamics of nanotechnologybased therapeutic approaches and prove their biological consequences in human eyes. This review aims to summarize the literature concerning the advances in nanotechnology, specifically regarding ocular devices applied to the treatment of glaucoma.

B-cells play a pivotal role in primary Sjögren's syndrome (pSS) pathogenesis. We aim to (1) evaluate the distribution of B-lymphocyte subpopulations in pSS and Sicca patients, (2) establish cut-off points that discriminate pSS from controls, (3) evaluate the association between memory B-cells and phenotypic features in pSS. We included 57 pSS patients, 68 Sicca and 24 healthy controls. Circulating B-cells were characterized by flow cytometry as naïve and memory subsets and classified from Bm1 to Bm5. Compared to controls, pSS patients had lower percentages (29.5 vs 44.4%) and absolute numbers (47 vs 106 cells/µl) of memory B-cells. Through ROC curves, a cut-off of ≤ 58 total memory B-cells/µl yielded a specificity of 0.88 and a sensitivity of 0.60 for pSS, and was met by 59.6% of pSS patients, 38.8% of Sicca and 12.5% of controls. A cut-off of < 23.5 Switched-memory B-cells/µl yielded a specificity of 0.88 and a sensitivity of 0.54 and was met by 54.4% of pSS patients, 37.3% of Sicca and 12.5% of controls. In pSS, lower total memory B-cells count was associated with longer disease duration (14.3 vs 8.1 years, p = 0.006) and more active disease profile, as evaluated by the European League Against Rheumatism (EULAR) Sjögren's Syndrome Disease Activity Index (ESSDAI) (3.1 vs 1.4, p = 0.043). Decreased numbers of memory B-cells clearly discriminated pSS from controls and can also have prognostic value. It remains to be clarified whether Sicca patients with decreased memory B-cells represent pSS and if B-cell profiling could help in the diagnosis of pSS.

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Purpose: To study structural chorioretinal changes in tamoxifen-treated patients. Methods: Cross-sectional case–control study comparing structural chorioretinal aspects in tamoxifen-treated patients and healthy controls. Enhanced depth spectral domain optic coherence tomography with choroidal binarization and optic coherence tomography angiography were performed. Individual retinal layer thickness and chorioretinal vascular components were compared. Subgroup analysis regarding history of chemotherapy was performed. Results: Two hundred eyes of 100 TAM-treated patients (Group 1) and 80 eyes of 40 healthy controls (Group 2) were included. Of the 200 spectral domain optic coherence tomography scans from patients, 2 showed structural changes attributable to tamoxifen. Group 1 showed significantly lower values in choroidal parameters and in total retinal, ganglion cell layer, inner plexiform layer, outer nuclear layer, and retinal pigment epithelial thicknesses as well as an increased thickness in the outer plexiform layer. The subgroup not submitted to chemotherapy maintained significant reductions in total retinal thickness, ganglion cell layer, retinal pigment epithelium, outer nuclear layer, outer retinal layer, choroidal parameters, as well as an increased thickness in the outer plexiform layer, in comparison with Group 2. Conclusion: Subclinical structural retinal changes could indicate early retinal pigment epithelial and photoreceptor damage. The new finding of choroidal thinning could point toward another important pathophysiologic process in tamoxifen-induced toxicity.

Sjögren's syndrome (SjS) is characterized by lymphocytic infiltration of exocrine glands, i.e. autoimmune epithelitis. Lymphocytes are central in SjS pathogenesis, with B-cell hyperactivity mediated by T-cells. B-cells are main targets of Epstein-Barr virus (EBV) infection, a frequently-suggested trigger for SjS. We aimed to evaluate how the EBV infection modulates B and T-cell subsets in SjS, including as controls Rheumatoid arthritis patients (RA) and healthy participants (HC). SjS patients presented decreased CXCR5+T-cells, although IL21-secreting Tfh and Tfc cells were increased. Tfc were positively correlated with ESSDAI scores, suggesting their relevant role in SjS pathogenesis. As previously described, SjS patients showed expanded circulating naïve B-cell compartments. SjS patients had a higher incidence of EBV-EA-D-IgG+ antibodies, characteristic of recent EBV-infection/reactivation. SjS patients with past infection or recent infection/reactivation showed increased CXCR3+Th1 and CXCR3+Tfh1 cells compared to those without active infection. SjS patients with a recent infection/reactivation profile presented increased transitional B-cells compared to patients with past infection and increased plasmablasts, compared to those without infection. Our results suggest EBV-infection contributes to B and T-cell differentiation towards the effector phenotypes typical of SjS. Local lymphocyte activation at ectopic germinal centres, mediated by Tfh and Tfc, can be EBV-driven, perpetuating autoimmune epithelitis, which leads to gland destruction in SjS.