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Cited by 393

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

HMGB1 Develops Enhanced Proinflammatory Activity by Binding to Cytokines

Sha, Yonggang, Zmijewski, Jaroslaw, Xu, Zhiwei, Abraham, Edward·2008·The Journal of Immunology

Abstract

High mobility group box 1 protein (HMGB1), originally characterized as a nuclear DNA-binding protein, has also been described to have an extracellular role when it is involved in cellular activation and proinflammatory responses. In this study, FLAG-tagged HMGB1 was inducibly expressed in the presence of culture media with or without added IL-1β, IFN-γ, or TNF-α. HMGB1 purified from cells grown in culture media alone only minimally increased cytokine production by MH-S macrophages and had no effect on murine neutrophils. In contrast, HMGB1 isolated from cells cultured in the presence of IL-1β, IFN-γ, and TNF-α had enhanced proinflammatory activity, resulting in increased production of MIP-2 and TNF-α by exposed cells. IL-1β was bound to HMGB1 isolated from cells cultured with this cytokine, and purified HMGB1 incubated with recombinant IL-1β acquired proinflammatory activity. Addition of anti-IL-1β Abs or the IL-1 receptor antagonist to cell cultures blocked the proinflammatory activity of HMGB1 purified from IL-1β-exposed cells, indicating that such activity was dependent on interaction with the IL-1 receptor. These results demonstrate that HMGB1 acquires proinflammatory activity through binding to proinflammatory mediators, such as IL-1β.

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Crossref · 10.4049/jimmunol.180.4.2531

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Metadata

Authors
Sha, Y., Zmijewski, J., Xu, Z., & Abraham, E.
Venue
The Journal of Immunology
Published
2008-02
Volume
180
Issue
4
Pages
2531-2537
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
OpenAlex
W1490007860
Cited by
393
References
5
FWCI
25.86
Type
journal article
Language
en
Open access
closed

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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