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Updated: May 15, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
T helper 17 cells are involved in the local and systemic inflammatory response in community-acquired pneumonia
Marthe S Paats1, Ingrid M Bergen, Wessel E J J Hanselaar
1Department of Pulmonary Medicine, Erasmus MC Rotterdam, Rotterdam, The Netherlands.
Background:
Recent findings in mouse models suggest that T helper (Th)17 cells, characterised by production of interleukin (IL)-17A and IL-22, are involved in the immunopathogenesis of pneumonia.
Objective:
In this study, we aimed to identify the involvement of Th17 cells in human community-acquired pneumonia (CAP).
Design:
Within 24 h of admission, T cells from peripheral blood (n=39) and bronchoalveolar lavage (BAL, n=20) of CAP patients and of 10 healthy individuals were analysed by intracellular flow cytometry for the production of various cytokines, including IL-17A and IL-22. Peripheral blood T cells were also analysed 7 and 30 days after admission. Th17 cytokine profiles were correlated with pneumonia severity index and microbial aetiology.
Results:
In the BAL of CAP patients, proportions of IL-17A and IL-22 single positive, as well as IL-17A/IL-22 double positive CD4 T cells were significantly increased compared with healthy individuals. Significantly increased proportions of IL-17A/IL-22 double positive CD4 T cells in BAL were found in non-severe and severe CAP patients, as well as in pneumococcal and non-pneumococcal CAP. In the peripheral blood of CAP patients upon admission, we found significantly increased proportions of IL-17A/IL-22 double positive CD4 T cells. One week after admission, the proportions of these double positive cells were still significantly increased in CAP patients compared with healthy individuals.
Conclusions:
These data indicate that Th17 cells are engaged in the local and systemic immune response in human pneumonia. Especially, IL-17A/IL-22 double positive Th17 cells may be involved in the immunopathogenesis of CAP.
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