To examine the capacity of IL-11 to induce encephalitogenic Th17 cells. 

IL-11 is the most up-regulated cytokine in the serum and CSF samples from patients with clinically isolated syndrome (CIS) suggestive of multiple sclerosis (MS).  Studies of relapsing remitting experimental autoimmune encephalomyelitis (RREAE), confirmed a causative role of IL-11 in worsening clinical severity of the disease and inducing increased numbers of IL-17⁺CD4⁺ cells within the spinal cord inflammatory infiltrates. Passive transfer RREAE is used to directly examine the role of IL-11 in the induction of the encephalitogenic Th17 cells.

SJL Mice were immunized with PLP_139-151, sacrificed at day 11 at the onset of clinical EAE, and LN cells were re-stimulated with: 1) PLP, 2) PLP+IL-11, and 3) PLP+IL23 for 7 days. Clinical scores and weight were measured following passive transfer of CD4+ cells daily in three groups for 70 days.

Antigen recall experiments using LN cells revealed that in vitro restimulation with PLP _139-151 in the presence of IL-11 induces an increased percentage of IL-17A⁺CD4⁺ cells (17.80%, p<0.001), similar to IL-23 (18.33%, p<0.001).  Upon passive transfer of CD4⁺ cells, mice that received IL-11-stimulated cells had an earlier onset of the disease (day 9 vs. 14) and increased average scores compared to mice that received cells restimulated with antigen only (ANOVA, p<0.001). There was no statistically significant difference between the severity of the disease induced by IL-11 and IL-23-polarized cells.