Fig 1: Increased cellular expression of chemokine receptors CCR2, CCR5, and CXCR3 in O-PML CSF(A) Feature plots depict expression level and distribution of CCL2, CCL3, CCL4, CCL5, CCL20, CXCL10, CXCL13, and CXCL16 in CSF of combined scRNA-seq datasets.(B) Quantifications of the proportion of cells positive for CCL2, CCL3, CCL4, CCL5, CCL20, CXCL10, CXCL13, and CXCL16 as percentage of mononuclear cells (MNCs) per sample in the CSF of IIH (n = 9), RRMS (n = 12), RRMS-Nat (n = 5), O-PML (n = 3), and VE (n = 5) patients are shown.(C) Feature plots depict expression level and distribution of CCR2, CCR5, CCR20, CXCR3, CXCR5, and CXCR6 in CSF of combined scRNA-seq datasets.(D) Quantifications of the proportion of cells positive for CCR2, CCR5, CCR20, CXCR3, CXCR5, and CXCR6 as percentage of cell in the lineage cluster per lineage and sample in the CSF of IIH patients, RRMS patients, RRMS-Nat patients, O-PML patients, and VE patients are shown. Boxplots show the IQR, with whiskers indicating IQR x 1.5, line denoting the median, and “+” indicating the mean. Statistical differences between IIH and O-PML were computed using Wilcoxon tests. In case of significant differences, statistical difference between IIH and RRMS and IIH and VE was also computed. ∗p < 0.05, ∗∗p < 0.01. IIH, idiopathic intracranial hypertension; RRMS, treatment-naïve RRMS patients; RRMS-Nat, natalizumab-treated RRMS patients; O-PML, non-MS patients at time of non-natalizumab-associated PML diagnosis; VE, viral encephalitis patients.