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Alternative splicing directs two IL-20R2 isoforms and is responsible for the incomplete gene knockout via the exon I ablation


Two heterodimeric receptors consisting of interleukin (IL)-20R2 are shared by three of the IL-20 family of cytokines, IL-19, IL-20 and IL-24. Along with IL-22, these cytokines are downstream effectors of IL-23 and have been implicated in keratinocyte functions and the pathogenesis of psoriasis. Surprisingly, whereas knocking out either the IL-23 or IL-22 gene abolished imiquimod-induced psoriatic phenotypes in mice, similar attempt for IL-20R2 had little effect. Here, we report that the apparent disparity may result from a new IL-20R2 isoform encoded by an alternatively spliced transcript which survived the previous attempt for IL-20R2 gene knockout via the exon I deletion.

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We would like to thank Dr Ursula Maria Wegenka for making the IL-20R2 knockout mice available and her kind advice for this study. This work was supported in part by a 863 grant (2012AA02A305) and grants (2012ZX09103301; 2011ZX09401005) from the Chinese Ministry of Science and Technology (PL), a 973 grant (2012CB910700) from the Chinese Ministry of Education (PL), and a grant (81171955) from the Chinese Natural Science Foundation (PL). We thank Jamie Walden and Jonathan Meade from GenHunter Corporation for proofreading the manuscript.

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Correspondence to P Liang.

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Zhou, H., Liu, X., Yu, R. et al. Alternative splicing directs two IL-20R2 isoforms and is responsible for the incomplete gene knockout via the exon I ablation. Genes Immun 17, 220–227 (2016).

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