Figure 7. H₁R signaling directly in CD4⁺ T cells regulates encephalitogenic Th1 effector responses.

Clinical EAE course (A and B), severity of CNS pathology (C and D), and ex vivo cytokine responses (E and F) of WT, H1RKO, and H1RKO-Tg mice were compared following immunization with MOG_35–55-CFA plus PTX (A, C, and E) or 2× MOG_35–55 and CFA (B, D, and F). Cytokine production was assessed by stimulating splenocytes with MOG_35–55 on day 10 after injection, and supernatants were collected and quantified by ELISA in triplicate. The significance of differences in the course of clinical disease, CNS pathology indices, and cytokine responses were assessed by regression analysis (63), χ² test, or ANOVA followed by Bonferroni corrected post-hoc comparisons. With the exception of TNF-α and IL-17 production, significant differences among the strains were detected for all parameters at P < 0.0001 — WT, H1RKO-Tg1, and H1RKO-Tg3 groups were equivalent and all significantly different from the H1RKO group.