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SARS-CoV-2 specific T cell responses are lower in children and increase with age and time after infection

SARS-CoV-2 infection of children leads to a mild illness and the immunological differences with adults are unclear. Here, we report SARS-CoV-2 specific T cell responses in infected adults and children and find that the acute and memory CD4(+) T cell responses to structural SARS-CoV-2 proteins increa...

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Detalles Bibliográficos
Autores principales: Cohen, Carolyn A., Li, Athena P. Y., Hachim, Asmaa, Hui, David S. C., Kwan, Mike Y. W., Tsang, Owen T. Y., Chiu, Susan S., Chan, Wai Hung, Yau, Yat Sun, Kavian, Niloufar, Ma, Fionn N. L., Lau, Eric H. Y., Cheng, Samuel M. S., Poon, Leo L. M., Peiris, Malik, Valkenburg, Sophie A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8322064/
https://www.ncbi.nlm.nih.gov/pubmed/34326343
http://dx.doi.org/10.1038/s41467-021-24938-4
Descripción
Sumario:SARS-CoV-2 infection of children leads to a mild illness and the immunological differences with adults are unclear. Here, we report SARS-CoV-2 specific T cell responses in infected adults and children and find that the acute and memory CD4(+) T cell responses to structural SARS-CoV-2 proteins increase with age, whereas CD8(+) T cell responses increase with time post-infection. Infected children have lower CD4(+) and CD8(+) T cell responses to SARS-CoV-2 structural and ORF1ab proteins when compared with infected adults, comparable T cell polyfunctionality and reduced CD4(+) T cell effector memory. Compared with adults, children have lower levels of antibodies to β-coronaviruses, indicating differing baseline immunity. Total T follicular helper responses are increased, whilst monocyte numbers are reduced, indicating rapid adaptive co-ordination of the T and B cell responses and differing levels of inflammation. Therefore, reduced prior β-coronavirus immunity and reduced T cell activation in children might drive milder COVID-19 pathogenesis.