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Children's immune cells may explain all their illnesses

New research shows immune systems of young mice secrete low levels of the cytokine — CD4 T — needed for survival during infection. By comparison, older mice secret more.


Schools are commonly known as breeding grounds for viruses and bacteria, but this may not simply represent poor hygiene. New research in mice shows children's immune systems do not operate with the same efficiency as adults. Children may not only be more likely to contract viral infections, but also take to longer clear them.

Specifically, the study examined how CD4 T-cells (immune cells key in fighting viral infection) respond to influenza. Researchers found that children's immune systems may not be able to make sufficient antibody molecules to rid their lungs of influenza virus as quickly as adults. The findings were reported July 2016 in the Journal of Leukocyte Biology.


"Our hope is that understanding the key differences in the immune responses of young children, we may be able to develop better ways to bolster their immunity toward common pathogens affecting them.

"More importantly, this knowledge may help us consider new designs of current vaccines, since adult and children's immune systems respond to them in different ways."


David E. Verhoeven PhD, Research Assistant Professor, College of Veterinary Medicine, Iowa State University, Ames, Iowa, USA.


To make this discovery, scientists used two groups of mice to model the effects of influenza infection in young children and adults. The first group was 21 days old, and the second group 8-10 weeks old. Both groups were infected with influenza virus, strain H1N1.

Researchers then compared their immune responses to infection. They found that CD4 T-cells in young mice secreted a key antiviral cytokine, interferon gamma, at significantly lower levels than adult CD4 T-cells.


Lower levels of interferon gamma led to higher rates of CD4 T-cell death during infection. Because CD4 T-cells are involved in antibody production, young mice were unable to mount a strong immune response to clear the virus from their lungs until very late.


"Anyone with young children knows that they bring home all sorts of germs and infections, and in fact, children can be a major source of epidemiological spread of some infections," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology. "These new data are important because they start to point at key immune mechanisms that operate differently at young ages that might allow delays in viral clearance which could translate to longer ability to transmit such infections to new hosts."

Abstract
Respiratory viral infections, such as influenza, can lead to delayed viral clearance in toddlers, possibly exacerbating disease morbidity. We hypothesized that defective CD4 T cells in toddlers may contribute to a failure to clear virus at a similar rate to adults. Thus, we developed a young mouse model to examine potential divergent responses between toddlers and adults. We determined that young mice (toddler mice, 21 d old) were actively generating and recruiting effector/memory T cells, whereas memory populations were firmly established in older, adult mice (8–10 wk old). We infected toddler and adult mice with influenza A/PR8/34 (H1N1) and found young mice had elevated morbidity, as measured by enhanced weight loss and lower partial pressure of oxygen levels, throughout the infection, thus, modeling the higher morbidity observed in children (<2 y old) during infection. Early viral loads were comparable to adult mice, but toddler mice failed to clear virus by 10 d postinfection. This delayed clearance corresponded to poor lung recruitment of CD4 T cells, lower antiviral T cell responses, and lower B cell/antibodies in the lungs. Mechanistically, diminished interferon-γ was detected in the lungs of toddler mice throughout the infection and corresponded to intrinsic, rather than extrinsic, CD4 T cell limitations in interferon-γ transcription. Moreover, defects in interferon-γ production appeared downstream from signal transducer and activator of transcription 4 in the interleukin-12 signaling pathway, suggesting maturational delays different from neonates. Importantly, recombinant interferon-γ supplementation rescued CD4 T cell numbers in the lungs and influenza-specific antibody formation. This study highlights the intrinsic limitations in CD4 T cell effector functions that may arise in toddlers and contribute to disease pathology.

David Verhoeven, Sheldon Perry, and Karin Pryharski. Control of influenza infection is impaired by diminished interferon-γ secretion by CD4 T cells in the lungs of toddler mice. J. Leukoc. Biol. July 2016, 100:203-212; doi:10.1189/jlb.4A1014-497RR ; http://www. jleukbio. org/ content/ 100/ 1/ 203. abstract ; Early online: January 28, 2016. Final: June 30, 2016

The Journal of Leukocyte Biology publishes peer-reviewed manuscripts on original investigations focusing on the cellular and molecular biology of leukocytes and on the origins, the developmental biology, biochemistry and functions of granulocytes, lymphocytes, mononuclear phagocytes and other cells involved in host defense and inflammation. The Journal of Leukocyte Biology is published by the Society for Leukocyte Biology.
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Jul 7, 2016   Fetal Timeline   Maternal Timeline   News   News Archive   



Children's immune systems may not be able to make sufficient antibody
molecules to rid their lungs of influenza virus as quickly as adults..
Image Credit: Public Domain


 


 

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