AI Article Synopsis
- Recent studies highlight that IL-17 can be helpful in fighting pathogens, but too much IL-17 is linked to chronic inflammation and autoimmune diseases.
- This research used special mice to observe how IL-17A is produced during infections, finding that it is produced by certain T cells during bacterial infections, but not in response to viral infections or type 1 diabetes.
- The results suggest that IL-17A is not necessary for viral elimination and the development of type 1 diabetes, challenging its perceived importance in these conditions.
Article Abstract
Recent studies have shown that IL-17 can contribute beneficially to pathogen defense but also that excessive IL-17 levels are associated with chronic inflammation and autoimmune disorders. To date, the role of IL-17 in viral infections and type 1 diabetes is ambiguous. In this study, we used IL-17A enhanced green fluorescent protein bicistronic reporter mouse strains to analyze in situ production of IL-17A. Upon Klebsiella pneumoniae bacterial infection, CD4(+) and γδ T cells produce IL-17A. In contrast, CD4(+) or CD8(+) T cells do not produce IL-17A in response to acute or protracted viral infection with lymphocytic choriomeningitis virus or during autoimmune diabetes development in the CD8-driven lymphocytic choriomeningitis virus-induced model of type 1 diabetes. We conclude that viral elimination and type 1 diabetes can occur in the absence of detectable IL-17A production, suggesting IL-17A is not essential in these settings.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3169711 | PMC |
| http://dx.doi.org/10.4049/jimmunol.1000180 | DOI Listing |
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