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Updated: Dec 21, 2025
An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
Innate Type 2 Responses to Respiratory Syncytial Virus Infection
Allison E Norlander1, R Stokes Peebles1
1Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232-2650, USA.
Insights
Respiratory syncytial virus (RSV) can cause severe infant bronchiolitis and later asthma. Group 2 innate lymphoid cells (ILC2) and alarmins drive type 2 immunity, offering potential therapeutic targets for severe RSV disease.
Area of Science:
- Immunology
- Pediatrics
- Infectious Diseases
Background:
- Respiratory syncytial virus (RSV) is a leading cause of infant hospitalization.
- Severe RSV bronchiolitis is linked to childhood asthma development.
- RSV infection typically elicits a type 1 immune response, but type 2 cytokines are also involved.
Purpose of the Study:
- To review the role of group 2 innate lymphoid cells (ILC2) in RSV infection.
- To explore the function of epithelial-derived alarmins (IL-33, IL-25, TSLP, HMGB1) in activating ILC2 during RSV.
- To discuss the therapeutic potential of targeting the innate type 2 inflammatory pathway in severe RSV disease.
Main Methods:
- Literature review focusing on innate lymphoid cells and cytokine responses in RSV.
- Analysis of the mechanisms by which alarmin proteins activate ILC2.
- Synthesis of evidence linking type 2 immunity to severe RSV outcomes and asthma risk.
Main Results:
- Group 2 innate lymphoid cells (ILC2) are implicated in the type 2 immune response during RSV infection.
- Epithelial-derived alarmins, including IL-33, IL-25, TSLP, and HMGB1, activate ILC2.
- ILC2 activation promotes type 2 cytokine production, contributing to RSV pathogenesis.
Conclusions:
- The innate type 2 inflammatory pathway involving ILC2 and alarmins plays a significant role in severe RSV disease.
- Targeting this pathway presents a potential therapeutic strategy for managing severe RSV infections in infants.
- Understanding ILC2's role may offer insights into the link between severe RSV and later asthma development.
Abstract:
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.
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