Pattern recognition receptor-mediated cytokine response in infants across 4 continents? - 01/03/14
Abstract |
Background |
Susceptibility to infection as well as response to vaccination varies among populations. To date, the underlying mechanisms responsible for these clinical observations have not been fully delineated. Because innate immunity instructs adaptive immunity, we hypothesized that differences between populations in innate immune responses may represent a mechanistic link to variation in susceptibility to infection or response to vaccination.
Objective |
Determine whether differences in innate immune responses exist among infants from different continents of the world.
Methods |
We determined the innate cytokine response following pattern recognition receptor (PRR) stimulation of whole blood from 2-year-old infants across 4 continents (Africa, North America, South America, and Europe).
Results |
We found that despite the many possible genetic and environmental exposure differences in infants across 4 continents, innate cytokine responses were similar for infants from North America, South America, and Europe. However, cells from South African infants secreted significantly lower levels of cytokines than did cells from infants from the 3 other sites, and did so following stimulation of extracellular and endosomal but not cytosolic PRRs.
Conclusions |
Substantial differences in innate cytokine responses to PRR stimulation exist among different populations of infants that could not have been predicted. Delineating the underlying mechanism(s) for these differences will not only aid in improving vaccine-mediated protection but possibly also provide clues for the susceptibility to infection in different regions of the world.
Le texte complet de cet article est disponible en PDF.Key words : Innate immunity, immune development, infectious disease, global
Abbreviations used : LPS, MDP, NOD, PCA, PGN, Poly I:C, PRR, R848, TLR
Plan
| ☆ | This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
| T.R.K. is supported in part by a Career Award in the Biomedical Sciences from the Burroughs Wellcome Fund, and a Michael Smith Foundation for Health Research Career Investigator Award. D.P.S. is a Sauder Family Professor of Pediatric Infectious Diseases. P.J.C is supported by the Wellcome Trust (088862/Z/09/Z). A.M. is a senior research associate at the Belgian Fund for Scientific Research. This work was in part supported by the BC Children’s Hospital (BCCH) Foundation and CIHR CMF-108029. |
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| Disclosure of potential conflict of interest: E. S. Fortuno has received research support from the Burroughs Wellcome Fund (BWF). W .W. Mohn has received research support from the Canadian Institutes of Health Research and the Tula Foundation. P. J. Cooper has received research support from the Wellcome Trust. M. Esser is employed by the National Health Laboratory Systems. A. Marchant has received research support from GSK Biologicals, has received consultancy fees from GSK Biologicals and Hookipa, and is employed by ImmuneHealth. T. R. Kollmann has received research support from the BCCH Foundation, Canadian Institutes of Health Research (CIHR), Department of Defense (DOD), National Institutes of Health, and ADVAXIS, Inc, and has received travel support from the BCCH Foundation. The rest of the authors claim that they have no relevant conflicts of interest. |
Vol 133 - N° 3
P. 818 - mars 2014 Retour au numéro
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