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Milora KA, Uppalapati SR, Sanmiguel JC, Zou W, Jensen LE
Interleukin-36beta provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses
Sci Rep (2017) 7:5799.
Abstract
Interleukin-36 (IL-36) represents three cytokines, IL-36alpha, IL-36beta and IL-36gamma, which bind to the same receptor, IL-1RL2; however, their physiological function(s) remain poorly understood. Here, the role of IL-36 in immunity against HSV-1 was examined using the flank skin infection mouse model. Expression analyses revealed increased levels of IL-36alpha and IL-36beta mRNA in infected skin, while constitutive IL-36gamma levels remained largely unchanged. In human keratinocytes, IL-36alpha mRNA was induced by HSV-1, while IL-1beta and TNFalpha increased all three IL-36 mRNAs. The dominant alternative splice variant of human IL-36beta mRNA was isoform 2, which is the ortholog of the known mouse IL-36beta mRNA. Mice deficient in IL-36beta, but not IL-36alpha or IL-36gamma, succumbed more frequently to HSV-1 infection than wild type mice. Furthermore, IL-36beta-/- mice developed larger zosteriform skin lesions along infected neurons. Levels of HSV-1 specific antibodies, CD8+ cells and IFNgamma-producing CD4+ cells were statistically equal in wild type and IL-36beta-/- mice, suggesting similar initiation of adaptive immunity in the two strains. This correlated with the time at which HSV-1 genome and mRNA levels in primary skin lesions started to decline in both wild type and IL-36beta-/- mice. Our data indicate that IL-36beta has previously unrecognized functions protective against HSV-1 infection.
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Publication Date: 2017-07-19.
PMCID: PMC5517484
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Last updated on Wednesday, September 06, 2017