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.
Highlights
Infection by respiratory syncytial virus (RSV) affects approximately 33 million infants annually worldwide and is a major cause of hospitalizations
Th17 lymphocytes are important contributors to both protective immune responses and the pathology associated with RSV infection
The involvement of Th17 cells in the patho-physiology that accompanies RSV infections is of great topical interest
Summary
Th17 lymphocytes play a central role in host defences against a range of extracellular pathogens including bacteria, viruses and fungi [1,2,3]. The production of low-levels of IL-17 by resident Th17 lymphocytes is necessary for maintaining immunological homeostasis in the gut This occurs under the influence of IL-1 and transforming growth factor beta (TGFβ) that are produced by gut epithelial cells [15]. Recent studies have revealed that low level CD3/TCR engagement, as compared with high level receptor engagement, preferentially promotes human Th17 differentiations and the effect is mediated through activating the NFAT-1 transcription factor [19,20]. The production of IL-23, in contrast, is associated with the expansion of Th17 lymphocytes in pathogenic settings such as in autoimmune disease [23] In this respect, IL-23 production by DCs during RSV infection has been suggested to be responsible for Th17 propagation and exacerbated inflammation associated with the infection [24,25]
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