Fig. 3.

scRNA-seq and flow cytometry analyses identify specific immune cell changes in PBMCs exposed in vitro to HSA.

(A) UMAP of 1,946 patients’ B cells exposed to HSA and the vehicle, colored by cell types. (B) Overlay of HSA and vehicle exposure on the B lymphocyte UMAP. (C) Box plots for the proportion of B cell populations that significantly changed after HSA exposure. (D, E) Scatterplots of the flow cytometry analysis showing the gating strategy to identify B and transitional B cells and boxplots showing their proportions after HSA exposure. (F) UMAP of 21,819 patients’ myeloid cells exposed to HSA and the vehicle, colored by cell populations. (G) Overlay of HSA and vehicle exposure on the myeloid cell UMAP. (H) Box plots for the proportion of myeloid cell types that significantly changed after HSA exposure. (I) UMAP of 12,692 patients’ CD4⁺ T cells exposed to HSA and the vehicle, colored by cell types. (J) Overlay of HSA and vehicle exposure on CD4⁺ T cell UMAP. (K) Box plots for the proportion of CD4⁺ T cells that significantly changed after HSA exposure. Fig. 3A–C and F–K have been designed using scRNA-seq in PBMCs from nine patients with AD cirrhosis. (D) and (E) were designed based on results obtained by flow cytometry in PBMCs from 10 age-matched HV. Significant differences between groups were assessed using paired t tests. AD, acutely decompensated; HSA, human serum albumin; HV, healthy volunteers; PBMC, peripheral blood mononuclear cell; pDC, plasmacytoid dendritic cell; scRNA-seq, single-cell RNA sequencing; UMAP, Uniform Manifold Approximation and Projection.