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. 2021 Feb 22;6(4):e142376. doi: 10.1172/jci.insight.142376

Figure 4. Therapeutic administration of LLL12b significantly suppresses EAE progression.

Figure 4

(A–C) Splenocytes from Vα2.3/Vβ8.2 TCR transgenic mice were activated with MBP Ac1-11 plus IL-6 for 3 days (d) and injected into naive B10.PL mice. LLL12b (10 mg/kg) or vehicle control were injected i.p. into mice daily for 7d starting on d10 after adoptive transfer. Peak clinical scores (control, n = 41; LLL12b, n = 34) and AUC (n = 3) were compared (A). On d25 after adoptive transfer, Tregs in the spleens were determined by intracellular staining (control, n = 16; LLL12b, n = 15) (B). Splenocytes (control, n = 10; LLL12b, n = 9) (B) and CNS infiltrating cells (C) were activated with MBP Ac1-11 for 3d (B) or overnight (C). IL-17 was determined by intracellular staining, gating on CD4+CD44+. (D and E) C57BL/6 mice were immunized with MOG 35-55 and treated with LLL12b (or control) as described in A starting on d14 after immunization. On d29 after immunization, splenocytes were activated with MOG 35-55 for 3d. IL-17 in supernatant was determined by ELISA (control, n = 16; LLL12b, n = 17) (E). (F–H) SJL/J mice were immunized with PLP 139-151 and treated with LLL12b (or control) as described in A starting on d9 (F) or d22 (G and H). Peak clinical scores (n = 34) and normalized AUC (n = 3) were compared (G). On d33 after immunization, splenocytes of mice in G were activated with PLP 139-151 for 3d. IL-17 in supernatant was determined by ELISA (LLL12b, n = 13; control, n = 15). EAE clinical scores were compared with Mann-Whitney U test. Bar graphs were compared with unpaired Student’s t test. Data represent mean ± SEM of 3–5 independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.