Journal
FRONTIERS OF MEDICINE
Volume 12, Issue 1, Pages 34-47Publisher
SPRINGER
DOI: 10.1007/s11684-017-0606-8
Keywords
influenza; innate T cells; CD4(+) and CD8(+) T cells; vaccination
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Funding
- Victoria India Doctoral Scholarship
- Melbourne International Fee Remission Scholarship (MIFRS), University of Melbourne
- Melbourne International Research Scholarships (MIRS)
- MIFRS
- NHMRC Program Grant [1071916]
- NHMRC
- Australian Government Department of Health
- National Health and Medical Research Council of Australia [1071916] Funding Source: NHMRC
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Influenza is a major global health problem, causing infections of the respiratory tract, often leading to acute pneumonia, life-threatening complications and even deaths. Over the last seven decades, vaccination strategies have been utilized to protect people from complications of influenza, especially groups at high risk of severe disease. While current vaccination regimens elicit strain-specific antibody responses, they fail to generate cross-protection against seasonal, pandemic and avian viruses. Moreover, vaccines designed to generate influenza-specific T-cell responses are yet to be optimized. During natural infection, viral replication is initially controlled by innate immunity before adaptive immune responses (T cells and antibody-producing B cells) achieve viral clearance and host recovery. Adaptive T and B cells maintain immunological memory and provide protection against subsequent infections with related influenza viruses. Recent studies also shed light on the role of innate Tcells (MAIT cells, gamma delta T cells, and NKT cells) in controlling influenza and linking innate and adaptive immune mechanisms, thus making them attractive targets for vaccination strategies. We summarize the current knowledge on influenza-specific innate MAIT and gamma delta Tcells as well as adaptive CD8(+) and CD4(+) Tcells, and discuss how these responses can be harnessed by novel vaccine strategies to elicit cross-protective immunity against different influenza strains and subtypes.
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