More Than Just Attractive: How CCL2 Influences Myeloid Cell Behavior Beyond Chemotaxis
Open accessAbstract
Monocyte chemoattractant protein-1 (MCP-1/CCL2) is renowned for its ability to drive the chemotaxis of myeloid and lymphoid cells. It orchestrates the migration of these cell types both during physiological immune defense and in pathological circumstances, such as autoimmune diseases including rheumatoid arthritis and multiple sclerosis, inflammatory diseases including atherosclerosis, as well as infectious diseases, obesity, diabetes, and various types of cancer. However, new data suggest that the scope of CCL2's functions may extend beyond its original characterization as a chemoattractant. Emerging evidence shows that it can impact leukocyte behavior, influencing adhesion, polarization, effector molecule secretion, autophagy, killing, and survival. The direction of these CCL2-induced responses is context dependent and, in some cases, synergistic with other inflammatory stimuli. The involvement of CCL2 signaling in multiple diseases renders it an interesting therapeutic target, although current targeting strategies have not met early expectations in the clinic. A better understanding of how CCL2 affects immune cells will be pivotal to the improvement of existing therapeutic approaches and the development of new drugs. Here, we provide an overview of the pleiotropic effects of CCL2 signaling on cells of the myeloid lineage, beyond chemotaxis, and highlight how these actions might help to shape immune cell behavior and tumor immunity.
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CCL2 influences lipid droplet biosynthesis and pro-inflammatory polarization, and can interact with other inflammatory mediators.
“CCL2 has been shown to influence LD biosynthesis [71] and pro-inflammatory polarization, and can interact with other inflammatory mediators [72].”
From Lipoprotein Lipase Regulates Microglial Lipid Droplet Accumulation (2021) · cites this paper as [72]
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- Authors
- Gschwandtner, M., Derler, R., & Midwood, K. S.
- Affiliations
- University of Oxford (GB)
- University of Graz (AT)
- Corresponding author
- Midwood, Kim S.
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2019-12-13
- Volume
- 10
- Pages
- 2759-2759
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC6923224
- OpenAlex
- W3005414324
- Cited by
- 611
- References
- 10
- Citations by year
- 2026: 52 · 2025: 101 · 2024: 101 · 2023: 108 · 2022: 111 · 2021: 98 · 2020: 40
- FWCI
- 5.93
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Austrian Science Fund
- Versus Arthritis
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- MCP-1, myeloid cells, chemotaxis, leukocyte adhesion, macrophage polarization, autophagy, cell killing, cell survival, inflammatory diseases, autoimmune disease, antitumor immunity, therapeutic target
- MeSH terms
- Animals, Cell Communication, Cell Differentiation, Chemotaxis, Gene Expression Regulation, Humans, Macrophage Activation, Macrophages, Signal Transduction, Chemokine CCL2, Myeloid Cells
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