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Special Focus: Vaccine Adjuvants - Review

Immunologic correlates of protection and potential role for adjuvants to improve influenza vaccines in older adults

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Pages 759-766 | Published online: 09 Jan 2014
 

Abstract

The decrease in influenza vaccine efficacy in the elderly is associated with a decline in the stimulation of cell-mediated and cytotoxic T-lymphocyte responses required for clinical protection against influenza, and may be particularly problematic when this population is administered split-virus vaccines that lack conserved viral proteins. Adjuvants, which act through innate immune mechanisms, are known to enhance both humoral and T-cell-mediated responses to influenza vaccines in this population. Adjuvant effects including enhanced antigen presentation, activation and maturation of dendritic cells and production of inflammatory cytokines can drive the desired cell-mediated immune responses. Toll-like receptor ligands comprise one class of adjuvants, which interact with external and internal receptors associated with dendritic cells and other APCs, leading to the regulation and production of important inflammatory cytokines. Potential advances in the production of more effective influenza vaccines for older people include the addition of adjuvants to standard split-virus vaccines and the use of alternate routes of vaccine delivery to augment the response to influenza infection. In this review, the authors discuss the impact of immune senescence on the response to influenza vaccination, the correlates of protection against influenza disease and the progress being made in the design of better influenza vaccines for the population aged 65 years and older.

Financial & competing interests disclosure

JE McElhaney has participated on advisory boards for GlaxoSmithKline, Sanofi Pasteur, Novartis, and Med-Immune, Merck and is on data monitoring boards for Sanofi Pasteur; she has received research grants from the Canadian Institutes of Health Research and the US National Institute of Allergy and Infectious Diseases, and has participated in clinical trials sponsored by Merck, GlaxoSmithKline and Sanofi Pasteur, has received honoraria and travel and accommodation reimbursements for presentations sponsored by Merck, GlaxoSmithKline and Sanofi Pasteur, and travel and accommodation reimbursements for participation on a publication steering committee for GlaxoSmithKline. The research was funded by grant number Grant Number: U01 AI074449 (PI: JEM) from the National Institutes of Health, National Institute of Allergy and Infectious Diseases. Funding of this work was also provided by the grant number 42387 from the Bill and Melinda Gates Foundation. RN Coler and SL Baldwin acknowledge the European Union’s Seventh Framework Programme (FP7/2007-2013) under grant agreement number 280873 ADITEC (IDRI grant) for continued related work in progress on a similar topic. The authors, SL Baldwin and RN Coler, are supported by their affiliate institutions. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

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