Transcriptional signatures of influenza A/H1N1-specific IgG memory-like B cell response in older individuals

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• 作者：Iana H. Haralambieva^a ; Inna G. Ovsyannikova^a ; Richard B. Kennedy^a ; Michael T. Zimmermann^b ; Diane E. Grill^b ; Ann L. Oberg^b ; Gregory A. Poland^a ; ^{poland.gregory@mayo.edu" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Influenza ; Human ; Influenza vaccines ; Vaccination ; Influenza A virus ; H1N1 subtype ; Enzyme-linked immunospot assay ; Sequence analysis ; RNA ; Gene expression ; B-lymphocytes ; Aging ; Immunity ; Humoral
• 刊名：Vaccine
• 出版年：2016
• 出版时间：25 July 2016
• 年：2016
• 卷：34
• 期：34
• 页码：3993-4002
• 全文大小：1610 K

文摘

Studies suggest that the recall-based humoral immune responses to influenza A/H1N1 originates from activated memory B cells. The aim of this study was to identify baseline, early and late blood transcriptional signatures (in peripheral blood mononuclear cells/PBMCs) associated with memory B cell response following influenza vaccination.

Methods

We used pre- and post-vaccination mRNA-Seq transcriptional profiling on samples from 159 subjects (50–74 years old) following receipt of seasonal trivalent influenza vaccine containing the A/California/7/2009/H1N1-like virus, and penalized regression modeling to identify associations with influenza A/H1N1-specific memory B cell ELISPOT response after vaccination.

Results

Genesets and genes (p-value range 7.92E⁻⁰⁸ to 0.00018, q-value range 0.00019–0.039) demonstrating significant associations (of gene expression levels) with memory B cell response suggest the importance of metabolic (cholesterol and lipid metabolism-related), cell migration/adhesion, MAP kinase, NF-kB cell signaling (chemokine/cytokine signaling) and transcriptional regulation gene signatures in the development of memory B cell response after influenza vaccination.

Conclusion

Through an unbiased transcriptome-wide profiling approach, our study identified signatures of memory B cell response following influenza vaccination, highlighting the underappreciated role of metabolic changes (among the other immune function-related events) in the regulation of influenza vaccine-induced immune memory.