Figure 6
Figure 6. The effect of B lineage–specific p16INK4 deletion on immune aging. (A) Representative flow analysis of B-cell homeostatic proliferation as measured by Ki-67 expression in resting B cells (CD40−) from spleens of mice with indicated ages and genotypes. (B) Quantification of K-i67 expression as shown in panel A. ns indicates not significant. **P < .01. (C) Representative flow analysis showing the effect of B-lineage p16INK4a deletion on antigen-specific B-cell proliferation. Mice were immunized and rechallenged with nitrophenylacetyl (see “NP immunization”) and BrdU incorporation in splenic B cells was measured in mice of indicated ages and genotypes. (D) Quantification of BrdU incorporation as shown in panel C; n = 4 mice per group, P values are as indicated.

The effect of B lineage–specific p16INK4 deletion on immune aging. (A) Representative flow analysis of B-cell homeostatic proliferation as measured by Ki-67 expression in resting B cells (CD40) from spleens of mice with indicated ages and genotypes. (B) Quantification of K-i67 expression as shown in panel A. ns indicates not significant. **P < .01. (C) Representative flow analysis showing the effect of B-lineage p16INK4a deletion on antigen-specific B-cell proliferation. Mice were immunized and rechallenged with nitrophenylacetyl (see “NP immunization”) and BrdU incorporation in splenic B cells was measured in mice of indicated ages and genotypes. (D) Quantification of BrdU incorporation as shown in panel C; n = 4 mice per group, P values are as indicated.

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