Objective: Chronic rhinosinusitis (CRS) is a heterogeneous disorder with distinct pathophysiologic mechanisms. Based on the transcription factor expression and cytokine production patterns in different types of innate lymphoid cells (ILCs), in parallel with those of adaptive CD4+ T helper (Th) cells and CD8+ cytotoxic T (Tc) cells, new perspectives on endotypes of patients are emerging around the immune response deviation into type 1 (orchestrated by ILC1s, Tc1 and Th1 cells), type 2 (characterized by ILC2s, Tc2 and Th2 cells), and type 3 (mediated by ILC3s, Tc17 and Th17 cells) responses. Additionally, cluster analysis has been applied to the endotyping of CRS in recent years, which has provided additional novel insights into the CRS pathogenesis. This article aims to review pathological mechanisms of CRS on the basis of type 1, type 2, and type 3 immune responses and how they inform us to begin to understand CRS endotypes. This article also reviews the recent cluster analysis studies of CRS endotypes. Finally, the impact of endotype on therapeutic management of CRS is summarized. Data Sources: Review of published literature. Study Selections: Relevant literature concerning CRS endotypes and the possible underlying mechanisms were obtained from a PubMed search and summarized here. Results and Conclusion: Both CRSwNP and CRSsNP are comprised of distinct endotypes with distinct deviated immune responses, pathogenic mechanisms, and different responses to medical and surgical treatment. An endotype of CRS with prominent type 2 immune responses is the most well studied endotype, and generally can benefit from treatment with steroids and specific type 2 disrupting biologics.

Nasal IL-4(+) TFH cells might be involved in local IgE production in eosinophilic nasal polyps.

The current outbreak of coronavirus disease 2019 (COVID-19), which was first reported in December 2019, spreads across the globe rapidly and has been declared as pandemic on 11 March 2020 by the World Health Organization. 1-4 COVID-19 is caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and associates with substantial morbidity and mortality. 2-8 As of 19 July 2020, more than 14.0 million cases have been confirmed and over 600,000 deaths. The clinical manifestations of COVID-19 are heterogeneous, ranging from asymptomatic to severe disease and even death. 9,10 Currently, no specific antiviral drug proved by randomized controlled trials or vaccine is available for the prevention and treatment of COVID-19. 8,10,11 A key challenge for clinicians is to identify risk and protective factors for COVID-19 to improve outcomes. A number of epidemiological studies have identified older age, male gender, black and minority ethnicity, and various comorbidities including hypertension,