September 18, 2013

Th17 Lymphocytes in Respiratory Syncytial Virus Infection

Viruses 20135(3), 777-791; doi:10.3390/v5030777
Review
1 Bone and Joint Research Unit, William Harvey Research Institute, Queen Mary University of London, London, EC1M 6BQ, UK2 Department of Rheumatology, The Royal London Hospital, Mile End, Barts and The London, Queen Mary University of London, London, EC1M 6BQ, UK
* Author to whom correspondence should be addressed.
Received: 23 January 2013; in revised form: 22 February 2013 / Accepted: 25 February 2013 / Published: 5 March 2013
(This article belongs to the Special Issue Pneumoviruses and Metapneumoviruses)
PDF Full-text Download PDF Full-Text [475 KB, Updated Version, uploaded 25 March 2013 11:53 CET]
The original version is still available [475 KB, uploaded 5 March 2013 16:19 CET]
Abstract: Infection by respiratory syncytial virus (RSV) affects approximately 33 million infants annually worldwide and is a major cause of hospitalizations. Helper T lymphocytes (Th) play a central role in the immune response during such infections. However, Th lymphocytes that produce interleukin 17 (IL-17), known as Th17 lymphocytes, in addition to been protective can also cause pathology that accompany this type of infection. The protective effects of Th17 is associated with better prognosis in most infected individuals but heightened Th17 responses causes inflammation and pathology in others. Studies employing animal models haves shown that activated Th17 lymphocytes recruit neutrophils and facilitate tertiary lymphoid structure development in infected lungs. However, IL-17 also inhibits the ability of CD8+ lymphocytes to clear viral particles and acts synergistically with the innate immune system to exacerbate inflammation. Furthermore, IL-17 enhances IL-13 production which, in turn, promotes the activation of Th2 lymphocytes and excessive mucus production. Studies of these animal models have also shown that a lack of, or inadequate, responses by the Th1 subset of T lymphocytes enhances Th17-mediated responses and that this is detrimental during RSV co-infection in experimental asthma. The available evidence, therefore, indicates that Th17 can play contradictory roles during RSV infections. The factors that determine the shift in the balance between beneficial and adverse Th17 mediated effects during RSV infection remains to be determined.
Keywords: RSV; pneumovirus; mucus; interleukin 17; interleukin 23; interleukin 13; Th17

No comments:

Post a Comment