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. Author manuscript; available in PMC: 2021 May 13.
Published in final edited form as: Crit Rev Immunol. 2020;40(4):297–309. doi: 10.1615/CritRevImmunol.2020034934

Figure 2: B cell responses shift to PR-dependent mechanisms with age.

Figure 2:

With age, humans and mice experience higher antigen exposure and an increased proinflammatory environment. Furthermore, the number of FOB, MZB and B1b/a cells decrease as ABC accumulate with age. This can be replicated in chronically infected and autoimmune-prone young mice, which accumulate CD11c+Tbet+ ABC. T-cell responses also decrease leading to a higher dependence on PR signals. Unlike, T-cell dependent FOB, ABC can be T-independent, and their activation depends on higher Ag exposure and PR signals. Thus, they can mount a primary response to new pathogens, which may provide protection.