Nicotine Inhibits Memory CTL Programming
Figure 6
Nicotine abolishes the regulatory function of rapamycin on memory programming.
Sorted OT-I cells were stimulated for 3 days with 3SI in the presence or absence of nicotine at 10 µM. Rapamycin was used in combination with or without nicotine. Cells were harvested and transferred into recipient B6 mice at a concentration of 106 cells/mouse. Memory CTLs were examined 40 days post-transfer. A. Comparison of memory CTLs in spleen. B. Comparison of the phenotype of memory CTLs in spleen. C. Comparison of memory protection against LM-OVA challenge in different memory mice in Panel A. D. Secondary expansion of memory CTLs 3 days post-LM-OVA challenge. These animals were the same as mentioned in Panel C. The results are representatives of two separate experiments with similar results. Asterisks indicate statistical significance. *, P<0.05; **, P<0.01; ***, P<0.001. E. Sorted OT-I cells were stimulated for 3 days with 3SI in the presence or absence of rapamycin, and expression of nAChRs was compared relatively to β1 in 3SI stimulation using quantitative PCR. Dotted lines in A and C indicate the detection limits. The results are representatives of two separate experiments with similar results.
