Figure 6.

CD8⁺ T cells from IL-4-deficient mice proliferate in response to endogenously produced IL-4.A. BALB/c congenic mice that express Thy 1.1 (4/gp) were immunized i.p. with 0.2 ml of saline or GaMD on d 0, boosted i.p. with 0.2 ml of saline or GaKLH on d 3, injected with spleen cells from wild-type, IL-4Rα-deficient, or IL-4-deficient BALB/c donors that contained 4.5 × 10⁶ CD8⁺ T cells on d 4, injected twice with BrdU on d 6, and sacrificed on d 7. Number and BrdU incorporation by donor (Thy1.2) splenic CD8⁺ T cells were determined by Coulter counting and flow cytometry. An asterisk indicated a significant response to GaMD/GaKLH compared to CD8⁺ T cells from GaMD/GaKLH-treated IL-4Rα-deficient mice in this experiment. Asterisks in the experiments shown in panels B and C similar indicate significant responses to GaMD or S. mansoni infection, respectively, by T cells from wild-type or IL-4-deficient mice as compared to T cells from IL-4Rα-deficient mice.

B. BALB/c IL-4Rα-deficient mice were immunized s.c. with GaMD on d 0 and injected with equal numbers of CFSE-labeled spleen cells from BALB/c wild-type, IL-4Ra-deficient, or IL-4-deficient mice on d 3 and sacrificed on d6. Numbers and proliferation indices (average number of cell divisions) of donor CD8⁺ T cells were determined by Coulter counting and flow cytometry.

C. BALB/c congenic mice that express Thy 1.1 were left untreated (n = 6) or inoculated with 60–70 S. mansoni cercaria on d 0 (n = 8) and injected with spleen cells from wild-type, IL-4Rα-deficient, or IL-4-deficient BALB/c donors that contained 3.5 × 10⁶ CD8⁺ T cells on d 39, injected twice with BrdU on d 52, and sacrificed on d 53. Number and BrdU incorporation by donor (Thy1.2) splenic CD8⁺ T cells were determined by Coulter counting and flow cytometry.