Characterization of main cytokine sources from the innate and adaptive immune responses following primary 17DD yellow fever vaccination in adults

Immunophenotyping on the molecular and cellular level is a central aspect for characterization of patients with inflammatory diseases, both to better understand disease etiopathogenesis and based on this to develop diagnostic and prognostic biomarkers which allow patient stratification and tailor-made treatment strategies. Technology-driven developments have considerably expanded the range of analysis tools. Especially the analysis of adaptive immune responses, often regarded as central though mostly poorly characterized disease drivers, is a major focus of personalized medicine. The identification of the disease-relevant antigens and characterization of corresponding antigen-specific lymphocytes in individual patients benefits significantly from recent developments in cytometry by sequencing and proteomics. The aim of this workshop was to identify the important developments for state-of-the-art immunophenotyping for clinical application and precision medicine. We focused here on recent key developments in analysis of antigen-specific lymphocytes, sequencing, and proteomics approaches, their relevance in precision medicine and the discussion of the major challenges and opportunities for the future.

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Characterization of Recombinant B. abortus Strain RB51SOD Toward Understanding the Uncorrelated Innate and Adaptive Immune Responses Induced byRB51SOD Compared to Its Parent Vaccine Strain RB51

Frontiers in Cellular and Infection Microbiology ◽

10.3389/fcimb.2011.00010 ◽

2011 ◽

Vol 1 ◽

Cited By ~ 1

Author(s):

Jianguo Zhu ◽

Charles B. Larson ◽

Megan Ann Ramaker ◽

Kimberly Quandt ◽

Jered M. Wendte ◽

...

Keyword(s):

Immune Responses ◽

Vaccine Strain ◽

Adaptive Immune Responses ◽

Adaptive Immune

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Characterization of homologous and heterologous adaptive immune responses in porcine reproductive and respiratory syndrome virus infection

Veterinary Research ◽

10.1186/1297-9716-43-30 ◽

2012 ◽

Vol 43 (1) ◽

pp. 30 ◽

Cited By ~ 46

Author(s):

Ivan Díaz ◽

Mariona Gimeno ◽

Laila Darwich ◽

Nuria Navarro ◽

Liudmila Kuzemtseva ◽

...

Keyword(s):

Virus Infection ◽

Immune Responses ◽

Respiratory Syndrome Virus ◽

Adaptive Immune Responses ◽

Adaptive Immune

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Yellow fever vaccine YF-17D activates multiple dendritic cell subsets via TLR2, 7, 8, and 9 to stimulate polyvalent immunity

Journal of Experimental Medicine ◽

10.1084/jem.20051720 ◽

2006 ◽

Vol 203 (2) ◽

pp. 413-424 ◽

Cited By ~ 376

Author(s):

Troy Querec ◽

Soumaya Bennouna ◽

Sefik Alkan ◽

Yasmina Laouar ◽

Keith Gorden ◽

...

Keyword(s):

Immune Responses ◽

Yellow Fever ◽

Yellow Fever Vaccine ◽

Interferon Α ◽

Adaptive Immune Responses ◽

Adaptive Immune ◽

Immunological Mechanisms ◽

History Of ◽

History Of Use ◽

Deficient Mice

The live attenuated yellow fever vaccine 17D (YF-17D) is one of the most effective vaccines available, with a 65-yr history of use in >400 million people globally. Despite this efficacy, there is presently no information about the immunological mechanisms by which YF-17D acts. Here, we present data that suggest that YF-17D activates multiple Toll-like receptors (TLRs) on dendritic cells (DCs) to elicit a broad spectrum of innate and adaptive immune responses. Specifically, YF-17D activates multiple DC subsets via TLRs 2, 7, 8, and 9 to elicit the proinflammatory cytokines interleukin (IL)-12p40, IL-6, and interferon-α. Interestingly, the resulting adaptive immune responses are characterized by a mixed T helper cell (Th)1/Th2 cytokine profile and antigen-specific CD8+ T cells. Furthermore, distinct TLRs appear to differentially control the Th1/Th2 balance; thus, whilst MyD88-deficient mice show a profound impairment of Th1 cytokines, TLR2-deficient mice show greatly enhanced Th1 and Tc1 responses to YF-17D. Together, these data enhance our understanding of the molecular mechanism of action of YF-17D, and highlight the potential of vaccination strategies that use combinations of different TLR ligands to stimulate polyvalent immune responses.

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