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Cell Immunol. 2017 Nov;321:52-60. doi: 10.1016/j.cellimm.2017.05.009. Epub 2017 Jul 11.

The properties of the unique age-associated B cell subset reveal a shift in strategy of immune response with age.

Author information

1
Department of Pathology, University of Massachusetts Medical School, United States. Electronic address: Susan.Swain@umassmed.edu.
2
Department of Pathology, University of Massachusetts Medical School, United States.

Abstract

In aged mice, conventional naive B cells decrease and a new population of age-associated B cells (ABC)3 develops. When aged unprimed mice are infected with influenza virus, there is a reduced generation of helper CD4 T cell subsets and germinal center B cells, leading to limited production of IgG Ab and less generation of conventional long-lived plasma cells, compared to young. However, we find an enhanced non-follicular (GL7-) ABC response that is helper T cell-independent, but requires high viral dose and pathogen recognition pathways. The infection-induced ABC (iABC) include IAV-specific Ab-secreting cells, some of which relocate to the bone marrow and lung, and persist for >4wk., suggesting they may provide significant protection. We also speculate there is a shift with increased age to dependence on TLR-mediated pathogen-recognition in both B and CD4 T cell responses.

KEYWORDS:

Aging; Antibody production; Antiviral response; B cell subsets; Immune response; Influenza virus; Pathogen recognition; T-independent response

PMID:
28712455
PMCID:
PMC5732074
DOI:
10.1016/j.cellimm.2017.05.009
[Indexed for MEDLINE]
Free PMC Article

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