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Identification of the IL-33 protein segment that controls subcellular localization, extracellular secretion, and functional maturation.

Abstract：

:Proteolytic activation of the IL-33 precursor, full-length interleukin-33 (FLIL33), at multiple sites within the sensor domain (aa 95-109) yields several functionally mature (MIL33) forms. Unlike nuclear FLIL33, intracellular MIL33 occurs in the cytoplasm, is secreted from source cells, and exerts biological effects by activating the ST2 receptor on target cells. Previous studies and our findings in this report indicated that IL-33 forms that are substantially longer than those produced by cleavage within the sensor domain are biologically indistinguishable from classical MIL33. We utilized a series of human and mouse N-terminal FLIL33 mutants to narrow down the boundaries of the nuclear localization sequence to aa 46-67, a segment known to include a portion of the chromatin-binding motif as well as another site controlling intracellular stability of FLIL33 in an importin-5-dependent fashion. The N-terminal FLIL33 deletion mutants starting prior to this region were intranuclear, non-secreted in cell culture, and manifested modest functional activity in vivo, similar to FLIL33. By contrast, the mutants starting after this region were cytoplasmic, secreted from cells in culture, and overtly biologically active in vivo, similar to MIL33. The deletion mutants starting within this region manifested an intermediate phenotype between FLIL33 and MIL33. Thus, this segment of IL-33 molecule controls multiple aspects of its biology, including subcellular localization, extracellular secretion, and functional maturation into the longest possible form of mature IL-33 cytokine. Future anti-IL-33 therapies may be based on interfering with this segment, thus restraining extracellular release and maturation of IL-33 into the active cytokine.

journal_name

Cytokine

journal_title

Cytokine

authors

Luzina IG,Clerman A,Fishelevich R,Todd NW,Lockatell V,Atamas SP

doi

10.1016/j.cyto.2019.02.015

subject

Has Abstract

pub_date

2019-07-01 00:00:00

pages

1-6

eissn

1043-4666

issn

1096-0023

pii

S1043-4666(19)30061-4

journal_volume

119

pub_type

杂志文章

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