Neutrophil extracellular traps are involved in enhanced contact hypersensitivity response in IL-36 receptor antagonist-deficient mice.

ABSTRACT: Loss-of-function homozygous or compound heterozygous mutations in IL36RN, which encodes interleukin-36 receptor antagonist (IL-36Ra), have been implicated in the pathogenesis of skin disorders. We previously reported that Il36rn^-/- mice exhibit an enhanced contact hypersensitivity (CHS) response through increased neutrophil recruitment. In addition, Il36rn^-/- mice show severe imiquimod-induced psoriatic skin lesions and enhanced neutrophil extracellular trap (NET) formation. We hypothesized that NETs may play an important role in the CHS response. To confirm this, we examined the CHS response and NET formation in Il36rn^-/- mice. Il36rn^-/- mice showed enhanced CHS responses, increased infiltration of inflammatory cells, including neutrophils, CD4<

SUBMITTER: Hasegawa Y 

PROVIDER: S-EPMC9352770 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature