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Aging has a strong impact on the activity of the immune system, enhancing susceptibility to pathogens and provoking a predominant pre-inflammatory status, whereas dampening responses to vaccines in humans and mice. Here, we demonstrate a loss of marginal zone B lymphocytes (MZ, CD19 + CD45R + CD21 ++ CD23 lo ) and a decrease of naive B cells (CD19 + IgD + ), whereas there is an enhancement of a CD19 + CD45R lo  innate-like B cell population (B1REL) and the so-called aged B cell compartment (ABC, CD45R + CD21 lo CD23 lo CD5 − CD11b − ) in aged senescence-accelerated (SAMP8) mice but not in aged senescence-resistant (SAMR1) mice. These changes in aged SAMP8 mice were associated with lower IgG isotype levels, displaying low variable gene usage repertoires of the immunoglobulin heavy chain (V H ) diversity, with a diminution on IgG1-memory B cells (CD11b − Gr1 − CD138 − IgM − IgD − CD19 + CD38 + IgG1 + ), an increase in T follicular helper (T FH , CD4 + CXCR5 + PD1 + ) cell numbers, and an altered MOMA-1 (metallophilic macrophages) band in primary follicles. LPS-mediated IgG1 responses were impaired in the B1REL and ABC cell compartments, both  in vitro  and  in vivo . These data demonstrate the prominent changes to different B cell populations and in structural follicle organization that occur upon aging in SAMP8 mice. These novel results raise new questions regarding the importance of the cellular distribution in the B cell layers, and their effector functions needed to mount a coordinated and effective humoral response.

Altered marginal zone and innate-like B cells in aged senescence-accelerated SAMP8 mice with defective IgG1 responses