Natural helper cells mediate respiratory syncytial virus-induced airway inflammation by producing type 2 cytokines in an IL-33-dependent manner

Immunotherapy ◽  
2017 ◽  
Vol 9 (9) ◽  
pp. 715-722 ◽  
Author(s):  
Xu Han ◽  
Ruonan Chai ◽  
Feifei Qi ◽  
Song Bai ◽  
Yulin Cui ◽  
...  
2004 ◽  
Vol 169 (10) ◽  
pp. 1167-1168 ◽  
Author(s):  
Keertan Dheda ◽  
Jim F. Huggett ◽  
Louise U. Kim ◽  
Alimuddin Zumla

Viruses ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 521 ◽  
Author(s):  
Allison E. Norlander ◽  
R. Stokes Peebles

Respiratory syncytial virus (RSV) is a common and contagious virus that results in acute respiratory tract infections in infants. In many cases, the symptoms of RSV remain mild, however, a subset of individuals develop severe RSV-associated bronchiolitis. As such, RSV is the chief cause of infant hospitalization within the United States. Typically, the immune response to RSV is a type 1 response that involves both the innate and adaptive immune systems. However, type 2 cytokines may also be produced as a result of infection of RSV and there is increasing evidence that children who develop severe RSV-associated bronchiolitis are at a greater risk of developing asthma later in life. This review summarizes the contribution of a newly described cell type, group 2 innate lymphoid cells (ILC2), and epithelial-derived alarmin proteins that activate ILC2, including IL-33, IL-25, thymic stromal lymphopoietin (TSLP), and high mobility group box 1 (HMGB1). ILC2 activation leads to the production of type 2 cytokines and the induction of a type 2 response during RSV infection. Intervening in this innate type 2 inflammatory pathway may have therapeutic implications for severe RSV-induced disease.


2019 ◽  
Vol 316 (1) ◽  
pp. L280-L290 ◽  
Author(s):  
Sisi Chen ◽  
Guangyuan Yu ◽  
Jun Xie ◽  
Wei Tang ◽  
Leiqiong Gao ◽  
...  

The type 2 immune response, induced by infection of respiratory syncytial virus (RSV), has been linked to asthma development, but it remains unclear how the response is initiated. Here, we reported that the high-mobility group box-1 (HMGB1) protein promotes the type 2 response in the later stage of RSV infection. In mice, we found that type 2 cytokines were elevated in the later stages, which were strongly diminished after administration of anti-HMGB1 antibodies. Further investigation revealed that HMGB1 expression was localized to CC10+ club cells in the lung. In the clinic, levels of HMGB1 in nasopharyngeal aspirates in hospitalized infants with RSV bronchiolitis [median (interquartile range) 161.20 ng/ml (68.06–221.30)] were significantly higher than those without lower respiratory tract infections [21.94 ng/ml (12.12–59.82); P < 0.001]. Moreover, higher levels of HMGB1 correlated with clinical severity. These results reveal a link between viral infection and the asthma-like type 2 responses that are associated with long-term consequences.


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