Fig. 9.
Fig. 9. Involvement of neutrophils in the allospecific TH1 response in MHC class II disparate mice. / (A) The anti-Gr1 neutrophil depletion inhibits the CD95L-dependent allospecific TH1 response. Bm12 mice were intraperitoneally injected with 5 × 105 lpr/lpr control or CD95L DCs and treated or not treated (NT) with control IgG or RB6-8C5 mAbs. After 5 days mesenteric LN cells were cultivated with syngeneic bm12 (white bars), allogeneic lpr/lpr (black bars), or third-party BALB/c (gray bars) spleen cells for 3 days. Supernatants were collected after 72 hours for IFN-γ quantification. Each group contains 3 to 7 individual mice. Results were expressed as mean ± SEM (*P = .0025; **P = .036). (B) Anti-GR1 mAbs treatment do not deplete the injected DC. DNA of mesenteric LNs was extracted, and the lpr/lpr mutation was detected by semiquantitative PCR. Results are means of lpr versus β-actin signals ± SEM of 4 mice/group (*P = .02). NS indicates not significant.

Involvement of neutrophils in the allospecific TH1 response in MHC class II disparate mice.

(A) The anti-Gr1 neutrophil depletion inhibits the CD95L-dependent allospecific TH1 response. Bm12 mice were intraperitoneally injected with 5 × 105 lpr/lpr control or CD95L DCs and treated or not treated (NT) with control IgG or RB6-8C5 mAbs. After 5 days mesenteric LN cells were cultivated with syngeneic bm12 (white bars), allogeneic lpr/lpr (black bars), or third-party BALB/c (gray bars) spleen cells for 3 days. Supernatants were collected after 72 hours for IFN-γ quantification. Each group contains 3 to 7 individual mice. Results were expressed as mean ± SEM (*P = .0025; **P = .036). (B) Anti-GR1 mAbs treatment do not deplete the injected DC. DNA of mesenteric LNs was extracted, and the lpr/lpr mutation was detected by semiquantitative PCR. Results are means of lpr versus β-actin signals ± SEM of 4 mice/group (*P = .02). NS indicates not significant.

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