Fig 2: CNS delivery of anti-CD52 mAb does not impact peripheral immune cells in healthy mice. Flow cytometric analysis of immune cell subsets in the spleen of healthy mice treated subcutaneously (a–d) or intrathecally (e–h) with vehicle (PBS, n = 5) or anti-CD52 mAb (n = 5). Data are depicted as absolute number of immune cell subsets (a, b, e, f), relative number of immune cell subsets (c, g), and percentage of IFNG+, IL17+, IL4+, and FOXP3+ cells in the CD4+ T cell pool (d, h). All replicates were biologically independent.Data are shown as mean ± SEM.*p < 0.05.**p < 0.01.

Fig 3: Oct-1/2 bind to the Il4 promoter and DHSs within the Th2 LCR.Binding of Oct-1/2 to the Il4 promoter (IL4P) and RHS5, RHS6, and RHS7 within the Th2 LCR was examined by a chromatin immunoprecipitation assay in Th1 and Th2 cells. Data are representative of three independent experiments with similar results. Statistical differences between groups were analyzed by Student’s t-test (*: P < 0.05).

Fig 4: PPAR? and lipid synthesis promote activation and IFN-? production of iNKT cells.a, b Surface CD69 (a), CD25 (b) on iNKT cells after activating by plate-coated anti-CD3 and anti-CD28 in the absence or presence of T007, Tofa. Unstimulated iNKT cells were used as negative controls. c Frequencies of Ki67+ iNKT cells after activating with plate-coated anti-CD3 and anti-CD28 for 2 days with or without T007, Tofa. d IFN-? and IL-4 production in iNKT cells activated by plate-coated mCD1d-PBS57 tetramer in the absence or presence of T007. e IFN-? and IL-4 production in iNKT cells in the absence or presence of Tofa as described in d. f, g mRNA of Ifng and Il4 in iNKT cells activated by anti-CD3 plus anti-CD28 for 24 h with or without antagonists of PPAR? (f) or fatty acid synthesis inhibitors (g). h, i Knockdown efficiency of Pparg shRNA (h) and its effect on percentages of IFN-?+ iNKT cells, after activating with plate-coated anti-CD3 and anti-CD28 (i). j PPAR? expression in iNKT cells or T cells from PLZF-cre Ppargfl/fl mice or Ppargfl/fl mice. k Percentages of IFN-?+ iNKT cells from PLZF-cre Ppargfl/fl mice or Ppargfl/fl mice, after activating with plate-coated anti-CD3 and anti-CD28 with or without T007, or PIO. Data are representative of six mice (j), or are means ± SEM of three independent experiments (h, i), nine biological replicates (a–e), four independent experiments (f, g), or six mice (k), pooled from three to four independent experiments. Data were analyzed by unpaired Student’s t-test (a–e) or Mann-Whitney test (f–i, k). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Source data are provided as a Source Data file.

Fig 5: Central nervous system delivery of anti-CD52 mAb impacts peripheral immune cells in experimental autoimmune encephalomyelitis (EAE) mice. Flow cytometric analysis of immune cell subsets in the spleen of EAE mice treated intrathecally at 10 days post-immunization (dpi) (a–c) or 20 dpi (d–f) with vehicle or anti-CD52 mAb (n = 4). Data are depicted as absolute number of immune cell subsets (a, d), relative number of immune cell subsets (b, e), and percentage of IFNG+, IL17+, IL4+, and FOXP3+ cells in the CD4+ T cell pool (c, f). All replicates were biologically independent.Data are represented as mean ± SEM.*p < 0.05.