Transient decrease in human peripheral blood myeloid dendritic cells following influenza vaccination correlates with induction of serum antibody

Abstract

Dendritic cells (DC) are critical inducers of the adaptive immune response. Extensive characterization of tissue-resident and monocyte-derived DC has revealed diverse stimulatory and regulatory actions, although the role of peripheral blood dendritic cells (PBDC) in maintaining homeostasis remains unclear. Examination of various myeloid (CD11c+CD303-) and plasmacytoid (CD11c-CD303+) DC populations in the peripheral blood of seasonal trivalent inactivated influenza vaccine recipients revealed a transient decrease in the frequency of CD11c+CD1c- myeloid DC subsets 5-10 days following vaccination, including both CD141+ and CD141- myeloid DC subsets of this population. These populations rebounded by 1 month, while plasmacytoid DC remained stable. The magnitude of the decrease in the CD141+ myeloid DC subset at d5-7 significantly correlated with the induction of influenza specific serum antibodies measured at 1 month following vaccination. These results demonstrate a mobilization of peripheral blood myeloid DC following vaccination and indicate these cells are potential biomarkers of immune response.

• Antibody
• blood
• dendritic cell
• human
• influenza
• vaccine

Acknowledgements

We extend our sincere gratitude to Ignacio Sanz for helpful discussions, Sally Quataert and the staff of the Rochester Human Immunology Center for sample processing and flow staining, Theresa Fitzgerald for performing the hemagglutination inhibition assays, Alexander Rosenberg for bioinformatics support, in addition to Benjamin Panepento, Li Zhang, Grace Chiu, and Jyh-Chiang E. Wang for technical support and the staff of the URMC Flow Cytometry Facility. The effort and commitment to the study demonstrated by the clinical coordinators and study participants is greatly appreciated.

This work was supported by the NIH/NIAID Rochester Center for the Biodefense of Immunocompromised Populations HHSN2662005500029C (N01-AI50029) and the University of Rochester Autoimmunity Center of Excellence (U19AI056390).

Dr. Kobie has received research support from Biogen Idec and Regeneron Pharmaceuticals. Dr. Ritchlin has received consulting fees, speaking fees, and/or honoraria from Abbott, Amgen, Boeringer Ingleheim, Janssen, UCB, Pfizer, and Celgene (less than $10 000 each). Dr. Treanor is on the scientific advisory board of Novartis, Immune Targeting Systems, and Visterra and has received grant support from Sanofi, Pfiser, GlaxoSmithKline, Vaxinnate, Protein Sciences, and Ligocyte. These relationships had no affect on the funding, conduct, or reporting of the submitted work. The authors alone are responsible for the content and writing of the paper.