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Research Paper|Volume 5, Issue 3|pp 209—226

B cell responses to the 2011/12-influenza vaccine in the aged

Raj K. Kurupati1, Senthil Kannan2, Xiang, Zhi Xiang1, Susan Doyle3, Sarah Ratcliffe4, Kenneth E. Schmader3, Hildegund CJ Ertl1
  • 1The Wistar Institute, Philadelphia, PA 19104, USA
  • 2Biomedical Graduate Group, University of Pennsylvania, Philadelphia, PA 19104, USA
  • 3GRECC, Durham VA Medical Center and Center for the Study of Aging and Human, Development and Division of Geriatrics, Department of Medicine, Duke University Medical Center, Durham NC 27710, USA
  • 4Department of Biostatistics and Epidemiology, University of Pennsylvania, Philadelphia, PA 19104, USA

* * Equal contribution

Received: October 2, 2012Accepted: March 20, 2013Published: March 25, 2013
https://doi.org/10.18632/aging.100541

Copyright: © 2013 Kurupati et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Antibody and B cell responses to influenza A viruses were measured over a period of 2 months in 30 aged and 15 middle-aged individuals following vaccination with the 2011/12 trivalent inactivated influenza vaccine by micro-neutralization assays, ELISAs, ELISpot assays and cell surface staining with lineage-defining antibodies followed by multicolor flow cytometry. Both cohorts developed comparable antibody responses to the H3N2 virus of the vaccine while responses to the H1N1 virus were compromised in the aged. ELISpot assays of peripheral blood mononuclear cells (PBMCs) gave comparable results for the two cohorts. Analysis by flow cytometry upon staining of CD19+IgD-CD20- PBMCs with antibodies to CD27 and CD38 showed markedly reduced increases of such cells following vaccination in the aged. Additional analysis of cells from a subset of 10 younger and 10 aged individuals indicated that in the aged a portion of IgG producing cells lose expression of CD27 and reduce expression of CD38.