Fig. 1: Immunophenotypic analysis of patients with ICI-induced SJS/TEN, ICI-induced mild cADR, and control participants. | Nature Communications

Fig. 1: Immunophenotypic analysis of patients with ICI-induced SJS/TEN, ICI-induced mild cADR, and control participants.

From: Immune checkpoint inhibitor-induced severe epidermal necrolysis mediated by macrophage-derived CXCL10 and abated by TNF blockade

Fig. 1

a Workflow showing sample collection and processing for 10X Genomics single-cell RNA sequencing (scRNA-seq) and the confirmation of results by flow cytometry, ex vivo lymphocyte activation test (LAT), BD Rhapsody scRNA-seq, ELISA/cytokine array, NanoString RNA-seq, and immunofluorescence assay performed in this study. Lesional blister cells (lesional BC) or peripheral blood mononuclear cells (PBMC) were obtained from enrolled patients with immune-related adverse events (irAEs) or control participants. b Characteristics of the participants enrolled in this study, such as groups with “immune checkpoint inhibitor (ICI)-cADR” (including ICI-induced Stevens-Johnson syndrome/toxic epidermal necrolysis [SJS/TEN], ICI-induced mild cADR) and “Control participants” (including small molecule drug-induced SJS/TEN, ICI-tolerant patients treated with ICI for at least 6 months with no evidence of drug-induced hypersensitivity reactions, burn patients, and healthy donors [HD] with no cADR history). Detailed clinical information can be found in Supplementary Table 1. c Representative clinical pictures of skin detachment for patients with ICI-induced SJS/TEN are shown. Other pictures of ICI-induced SJS/TEN (e.g., oral mucosal involvement and ocular injury) and ICI-induced mild cADR (lichenoid dermatitis) can be found in Supplementary Fig. 1a–l. d The identification of all cell clusters following 10X Genomics scRNA-seq of lesional BC and PBMC samples from patients with ICI-induced SJS/TEN, mild cADR and control participants (including lesional BC from 5 patients with ICI-induced SJS/TEN, PBMC from 5 the same patients with ICI-induced SJS/TEN, PBMC from 1 patient with an ICI-induced mild cADR [lichenoid dermatitis], and 5 each of sex-, age-matched ICI-tolerant patients and 6 of sex-, age-matched HD). A total of 115,327 cells are analyzed. e Violin plots show the expression of canonical marker genes across different clusters; the y-axis represents normalized values of marker gene expression (detailed gene expression profiles for different clusters can be found in Supplementary Fig. 1m). f Frequencies of cells in each cluster for each enrolled patient with ICI-cADR and control participants. ISB indicates ICI-induced SJS/TEN lesional BC; ISP indicates ICI-induced SJS/TEN PBMC; IMP indicates ICI-induced mild cADR (lichenoid dermatitis) PBMC; ITP indicates ICI-tolerant PBMC; HD indicates HD PBMC. g Distributions of all cell clusters colored for different groups of enrolled ICI-cADR patients and control participants. ISB: 18,010 cells; ISP: 22,156 cells; IMP: 6,354 cells; ITP: 34,477; HD: 34,330 cells. Figure 1a created with BioRender.com, released under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International license.

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