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REVIEW article

Front. Immunol.

Sec. Inflammation

This article is part of the Research TopicRecruitment of Leukocytes During Resolution of InflammationView all 5 articles

Chemokines in the resolution of inflammation: key players and targets for therapeutic modulation

Provisionally accepted
  • Laboratory of Molecular Immunology, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, KU Leuven, Leuven, Belgium

The final, formatted version of the article will be published soon.

The resolution of inflammation is an active, tightly regulated process essential for restoring tissue homeostasis after an inflammatory process. While chemokines are classically recognized for their roles in leukocyte recruitment and immune cell positioning during the onset of inflammation, emerging evidence highlights their pivotal functions in orchestrating the resolution phase, as well. The chemokine system contributes to inflammation resolution through several complementary mechanisms, including the depletion of pro-inflammatory chemokines, the generation of autoantibodies, the promotion of neutrophil reverse migration, the recruitment and polarization of pro-resolving immune cells such as macrophages and regulatory T cells, and the induction of tissue repair and disease recovery. Modulating chemokine-receptor interactions, enhancing the activity of pro-resolving chemokines, or blocking detrimental chemokine signaling pathways represent promising strategies for the treatment of excessive inflammation or chronic inflammatory diseases. In addition, modulation of glycosaminoglycan interactions or chemokine-modifying enzymes, might also be useful in this context. In this review, we explore the roles of chemokines in resolution, with a focus on their mechanistic contributions to immune modulation and their potential as therapeutic targets for restoring immune balance.

Keywords: Chemokines, Chemokine receptors, resolution of inflammation, immunemodulation, Leukocyte recruitment

Received: 02 Oct 2025; Accepted: 31 Oct 2025.

Copyright: © 2025 Oliveira, Proost and Struyf. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Vívian Louise Soares Oliveira, vivian.oliveira@kuleuven.be
Sofie Struyf, sofie.struyf@kuleuven.be

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