Immunity, Inflammation and Disease (Mar 2018)

T‐cell responses against rhinovirus species A and C in asthmatic and healthy children

  • Cibele M. Gaido,
  • Caitlyn Granland,
  • Ingrid A. Laing,
  • Peter N. Le Souëf,
  • Wayne R. Thomas,
  • Andrew J. Currie,
  • Belinda J. Hales

DOI
https://doi.org/10.1002/iid3.206
Journal volume & issue
Vol. 6, no. 1
pp. 143 – 153

Abstract

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Abstract Background Infections by rhinovirus (RV) species A and C are the most common causes of exacerbations of asthma and a major cause of exacerbations of other acute and chronic respiratory diseases. Infections by both species are prevalent in pre‐school and school‐aged children and, particularly for RV‐C, can cause severe symptoms and a need for hospitalization. While associations between RV infection and asthma are well established, the adaptive immune‐mechanisms by which RV infections influence asthma exacerbations are yet to be defined. Objective The aim of this study was to characterize and compare T‐cell responses between RV‐A and RV‐C and to test the hypothesis that T‐cell responses would differ between asthmatic children and healthy controls. Methods A multi‐parameter flow cytometry assay was used to characterize the in vitro recall T‐cell response against RV‐A and RV‐C in PBMCs from children with acute asthma (n = 22) and controls (n = 26). The responses were induced by pools of peptides containing species‐specific VP1 epitopes of RV‐A and RV‐C. Results Regardless of children's clinical status, all children that responded to the in vitro stimulation (>90%) had a similar magnitude of CD4+ T‐cell responses to RV‐A and RV‐C. However, asthmatic children had a significantly lower number of circulating regulatory T cells (Tregs), and healthy controls had significantly more Tregs induced by RV‐A than RV‐C. Conclusions and Clinical Relevance The comparable recall memory T‐cell responses in asthmatic and control children to both RV‐A and RV‐C show that differences in the antibody and inflammatory responses previously described are likely to be due to regulation, with a demonstrated candidate being reduced regulatory T‐cells. The reduced Treg numbers demonstrated here could explain the asthmatic's inability to appropriately control immunopathological responses to RV infections.

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