Background: New York City was the international epicenter of the COVID-19 pandemic. Health care providers responded by rapidly transitioning from in-person to video consultations. Telemedicine (ie, video visits) is a potentially disruptive innovation; however, little is known about patient satisfaction with this emerging alternative to the traditional clinical encounter. Objective: This study aimed to determine if patient satisfaction differs between video and in-person visits. Methods: In this retrospective observational cohort study, we analyzed 38,609 Press Ganey patient satisfaction survey outcomes from clinic encounters (620 video visits vs 37,989 in-person visits) at a single-institution, urban, quaternary academic medical center in New York City for patients aged 18 years, from April 1, 2019, to March 31, 2020. Time was categorized as pre–COVID-19 and COVID-19 (before vs after March 4, 2020). Wilcoxon-Mann-Whitney tests and multivariable linear regression were used for hypothesis testing and statistical modeling, respectively. Results: We experienced an 8729% increase in video visit utilization during the COVID-19 pandemic compared to the same period last year. Video visit Press Ganey scores were significantly higher than in-person visits (94.9% vs 92.5%; P<.001). In adjusted analyses, video visits (parameter estimate [PE] 2.18; 95% CI 1.20-3.16) and the COVID-19 period (PE 0.55; 95% CI 0.04-1.06) were associated with higher patient satisfaction. Younger age (PE –2.05; 95% CI –2.66 to –1.22), female gender (PE –0.73; 95% CI –0.96 to –0.50), and new visit type (PE –0.75; 95% CI –1.00 to –0.49) were associated with lower patient satisfaction. Conclusions: Patient satisfaction with video visits is high and is not a barrier toward a paradigm shift away from traditional in-person clinic visits. Future research comparing other clinic visit quality indicators is needed to guide and implement the widespread adoption of telemedicine.

Dendritic cells (DCs) play a key role in initiating immune responses and maintaining immune tolerance. In addition to playing a role in thymic selection, DCs play an active role in tolerance under steady state conditions through several mechanisms which are dependent on IL-10, TGF-β, retinoic acid, indoleamine-2,3,-dioxygenase along with vitamin D. Several of these mechanisms are employed by DCs in induction of regulatory T cells which are comprised of Tr1 regulatory T cells, natural and inducible foxp3+ regulatory T cells, Th3 regulatory T cells and double negative regulatory T cells. It appears that certain DC subsets are highly specialized in inducing regulatory T cell differentiation and in some tissues the local microenvironment plays a role in driving DCs towards a tolerogenic response. In this review we discuss the recent advances in our understanding of the mechanisms underlying DC driven regulatory T cell induction.

Gene transfer of CFTR cDNA to airway epithelia is a promising approach to treat cystic fibrosis (CF). Most gene transfer vectors use strong viral promoters even though the endogenous CFTR promoter is very weak. To learn whether expressing CFTR at a low level in a fraction of cells would correct Cl⁻transport, we mixed freshly isolated wild-type and CF airway epithelial cells in varying proportions and generated differentiated epithelia. Epithelia with ∼20% wild-type cells generated ∼70% the transepithelial Cl⁻current of epithelia containing 100% wild-type cells. These data were nearly identical to those previously obtained with CFTR expressed under control of a strong promoter in a CF epithelial cell line. We also tested high level CFTR expression using the very strong cytomegalovirus (CMV) promoter as well as the cytokeratin-18 (K18) promoter. In differentiated airway epithelia, the CMV promoter generated 50-fold more transgene expression than the K18 promoter, but the K18 promoter generated more transepithelial Cl⁻current at high vector doses. Using functional studies, we found that with marked overexpression, some CFTR channels were present in the basolateral membrane where they shunted Cl⁻flow, thereby reducing net transepithelial Cl⁻transport. These results suggest that very little CFTR is required in a fraction of CF epithelial cells to complement Cl⁻transport because transepithelial Cl⁻flow is limited at the basolateral membrane. Thus they suggest a broad leeway in promoter strength for correcting the CF gene transfer, although at very high expression levels CFTR may be mislocalized to the basolateral membrane.