Table I.

Defective NK cell function underlies the resistance to MOG35-55 peptide-induced EAE in IL-18−/− micea

Groups of MiceNo. of MiceTreatmentClinical Score ± SD (incidence)IFN-γ (pg/ml)TNF-α (pg/ml)
1. IL-18+/+4PBS3.3 ± 0.8 (4/4)367.4 ± 23302.2 ± 28
2. IL-18+/+6Control Ab+ IL-184.5 ± 1.1 (4/4)*482.0 ± 47*499.8 ± 47*
3. IL-18+/+6Anti-NK1.1+ IL-182.2 ± 0.6 (4/4)282.0 ± 22279.4 ± 35
4. IL-18−/−4PBS0.0 ± 0.0 (0/4)83.8 ± 33147.4 ± 55
5. IL-18−/−5Control Ab+ IL-182.8 ± 0.6** (4/5)310.4 ± 55*347.8 ± 29*
6. IL-18−/−6Anti-NK1.1 Ab + IL-181.6 ± 0.7 (2/5)112.5 ± 1488.9 ± 43
7. IL-18−/−5NK cells (RAG1−/−)2.1 ± 0.9* (4/5)322.1 ± 55*332.2 ± 14*
8. IL-18−/−5NK cells (RAG1/IFN−/−)0.5 ± 0.2* (1/5)107.6 ± 72*158.4 ± 33*
9. IL-18+/+8Anti-NK1.10.9 ± 0.7 (1/8)**145.8 ± 27*77.9 ± 34**
  • a Mice were treated with control (anti-mouse IgG) or anti-NK1.1 mAb (see Materials and Methods) 2 days before primary immunization with MOG35–55 peptide in CFA. All other manipulations were initiated at the day of primary immunization. EAE development was monitored until 25 days postimmunization (p.i.). Mice were subsequently sacrificed and CD4+ T cells from spleen were cultured. Cytokine production in response to the MOG35–55 peptide in culture supernatants were measured by ELISA. The range of cytokine spontaneous release: IFN-γ, 66 ± 47 pg/ml; TNF-α, 45 ± 30 pg/ml; IL-4, undetectable. No significant difference was found between WT and IL-18−/− mice. All results are expressed as mean values ± SD. Statistical evaluation was performed between experimental groups and corresponding control groups, respectively. *, p < 0.05; **, p < 0.01.