Fig. 4.
Fig. 4. CD95L-DCs promote a TH1 response in MHC class II–disparate mice. / CD95L-DCs exacerbated TH1 cytokines production in bm12 but not in lpr/lpr bm12 mice. 5 days after the subcutaneous footpad injection of 3 × 105 CD95L or control DCs draining popliteal and inguinal LN cells from bm12 (A) or lpr/lpr bm12 mice (B) were cultivated with bm12 (syngeneic, white bars), C57BL/6 lpr/lpr (allogeneic, black bars), or BALB/c (third-party, gray bars) spleen cells for 3 days. Supernatants were collected after 24 hours for IL-2 measurement and after 72 hours for IL-4, IL-5, and IFN-γ quantification. Results were expressed as mean ± SEM of 11 to 21 mice per groups of bm12 mice (*P ≤ .0001; **P = .0015; *** P = .03) and 3 mice per groups of lpr/lpr bm12 mice (NS: not significant with a 2-tailed Student t test). NT indicates nontreated mice.

CD95L-DCs promote a TH1 response in MHC class II–disparate mice.

CD95L-DCs exacerbated TH1 cytokines production in bm12 but not in lpr/lpr bm12 mice. 5 days after the subcutaneous footpad injection of 3 × 105 CD95L or control DCs draining popliteal and inguinal LN cells from bm12 (A) or lpr/lpr bm12 mice (B) were cultivated with bm12 (syngeneic, white bars), C57BL/6 lpr/lpr (allogeneic, black bars), or BALB/c (third-party, gray bars) spleen cells for 3 days. Supernatants were collected after 24 hours for IL-2 measurement and after 72 hours for IL-4, IL-5, and IFN-γ quantification. Results were expressed as mean ± SEM of 11 to 21 mice per groups of bm12 mice (*P ≤ .0001; **P = .0015; *** P = .03) and 3 mice per groups of lpr/lpr bm12 mice (NS: not significant with a 2-tailed Student t test). NT indicates nontreated mice.

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