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. 2019 Apr 8;129(5):1830–1832. doi: 10.1172/JCI128479

Figure 1. Single-cell RNA-seq–based identification of a role for FFAR3 in Th2 cells.

Figure 1

(A) T cells were isolated from esophageal biopsies obtained from subjects with EoE and healthy controls and analyzed by single-cell RNA-seq (scRNA-seq) on the Fluidigm C1 platform. (B) Two clusters of CD4+ T cells, T7 and T8, were enriched in subjects with EoE. (C) Cluster T8 included effector memory Th2 cells expressing IL4, IL5, and IL13, as well as FFAR3. Stimulation with FFAR ligands (SCFAs) increased production of Th2 cytokines in cell culture and augmented type 2 responses in an allergic airway disease model. In addition, IL-4 stimulated expression of FFAR3, suggesting the existence of a positive feedback loop that might amplify type 2 responses in EoE and other allergic diseases.