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  • IL-25 blockade augments antiviral immunity during respiratory virus infection.

IL-25 blockade augments antiviral immunity during respiratory virus infection.

Communications biology (2022-05-05)
Teresa C Williams, Su-Ling Loo, Kristy S Nichol, Andrew T Reid, Punnam C Veerati, Camille Esneau, Peter A B Wark, Christopher L Grainge, Darryl A Knight, Thomas Vincent, Crystal L Jackson, Kirby Alton, Richard A Shimkets, Jason L Girkin, Nathan W Bartlett
ABSTRACT

IL-25 is implicated in the pathogenesis of viral asthma exacerbations. However, the effect of IL-25 on antiviral immunity has yet to be elucidated. We observed abundant expression and colocalization of IL-25 and IL-25 receptor at the apical surface of uninfected airway epithelial cells and rhinovirus infection increased IL-25 expression. Analysis of immune transcriptome of rhinovirus-infected differentiated asthmatic bronchial epithelial cells (BECs) treated with an anti-IL-25 monoclonal antibody (LNR125) revealed a re-calibrated response defined by increased type I/III IFN and reduced expression of type-2 immune genes CCL26, IL1RL1 and IL-25 receptor. LNR125 treatment also increased type I/III IFN expression by coronavirus infected BECs. Exogenous IL-25 treatment increased viral load with suppressed innate immunity. In vivo LNR125 treatment reduced IL-25/type 2 cytokine expression and increased IFN-β expression and reduced lung viral load. We define a new immune-regulatory role for IL-25 that directly inhibits virus induced airway epithelial cell innate anti-viral immunity.

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Anti-Rabbit IgG (H+L), F(ab′)2 fragment, CF594 antibody produced in goat, ~2 mg/mL, affinity isolated antibody, buffered aqueous solution
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