Tuesday 3 October 2017

An article published this year in “Cell Death and Disease” using our “Apoptosis Detection Kit PE”, by our customers from the Instituto de Salud Carlos III (ISCIII), Majadahonda, Madrid, Spain,  in the analysis of how Altered marginal zone and innate-like B cells in aged senescence-accelerated SAMP8 mice with defective IgG1 responses. Congrats and Thanks.


Summay:
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++CD23lo) and a decrease of naive B cells (CD19+ IgD+ ), whereas there is an enhancement of a CD19+ CD45Rlo innate-like B cell population (B1REL) and the so-called aged B cell compartment (ABC, CD45R+ CD21loCD23loCD5−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 (VH) diversity, with a diminution on IgG1-memory B cells (CD11b−Gr1−CD138− IgM−IgD−CD19+ CD38+ IgG1+ ), an increase in T follicular helper (TFH, 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.
Reference:

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