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FEBS Lett. 2013 Oct 25. pii: S0014-5793(13)00776-X. doi: 10.1016/j.febslet.2013.10.019. [Epub ahead of print]

Interleukin-32δ interacts with IL-32β and inhibits IL-32β-mediated IL-10 production.

Author information

1
Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, 1 Hwayang-dong, Gwangjin-gu, Seoul 143-701, Republic of Korea.
2
Department of Biological Science, Sookmyung Women's University, Seoul 140-742, Republic of Korea. Tel.: +82-2-444-4218.
3
College of Pharmacy and Medical Research Center, Chungbuk National University, 12 Gashin-dong, Heungduk-gu, Cheongju, Chungbuk 361-463, Republic of Korea.
4
Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, 1 Hwayang-dong, Gwangjin-gu, Seoul 143-701, Republic of Korea. Electronic address: ydy4218@konkuk.ac.kr.

Abstract

There is growing evidence for multifunctional properties of IL-32. We previously demonstrated that IL-32β upregulates IL-10 production through the association with PKCδ. In this study, we examined the effects of other IL-32 isoforms on IL-10 production. We found that IL-32δ decreased IL-10 production and investigated the inhibitory mechanism of IL-32δ. We showed that IL-32δ suppressed IL-32β binding to PKCδ by interacting with IL-32β. The inhibitory effect of IL-32δ on IL-32β association with PKCδ was further verified by immuno-fluorescence staining. The co-localization of IL-32β and PKCδ around the nuclear membrane was disrupted by IL-32δ. Our data therefore indicate that IL-32δ plays an inhibitory role against IL-32β function, which also suggests that IL-32 may be regulated by its own isoform.

KEYWORDS:

IL-10; IL-32β; IL-32δ; Isoform interaction; PKCδ; U937

PMID:
24512848
DOI:
10.1016/j.febslet.2013.10.019
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