A Role for Macrophage Inflammatory Protein-3α/CC Chemokine Ligand 20 in Immune Priming During T Cell-Mediated Inflammation of the Central Nervous System
Open accessAbstract
Chemokines are a family of cytokines that exhibit selective chemoattractant properties for target leukocytes and play a significant role in leukocyte migration. In this study, we have investigated the role of the C-C chemokine, macrophage inflammatory protein (MIP)-3α/CC chemokine ligand 20, in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), a model of T cell-dependent inflammation. Expression in the CNS of MIP-3α, as determined by RT-PCR, increased in a time-dependent manner such that peak expression correlated with peak clinical disease. Similarly, levels of immunoreactive MIP-3α in the draining lymph nodes increased up to 10-fold 9 days postimmunization and remained elevated for up to 21 days postimmunization. The increased production of MIP-3α coincided with onset of clinical disease. Treatment of mice with specific neutralizing anti-MIP-3α Abs significantly reduced the severity of both clinical EAE and neuroinflammation by inhibiting the sensitization of lymphocytes to the specific Ag and release of lymphocytes from the draining lymph nodes. In contrast, adoptive transfer experiments indicated that MIP-3α was not essential for the effector phase of EAE. Together, these data demonstrate that MIP-3α plays a critical role in the sensitization phase of EAE.
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CCR6 is a chemokine receptor that promotes the recruitment of pathogenic T cells to inflammatory sites.
“CCR6 is a chemokine receptor that promotes the recruitment of pathogenic T cells to inflammatory sites (Hirota et al., 2007; Kohler et al., 2003).”
From Distinct characteristics of hippocampal pathogenic th17 cells in a mouse model of depression (2018) · cites this paper as Kohler et al., 2003
The introductory passage identifies CCR6 as a receptor for CCL20, a chemokine with in-vitro activity toward activated T cells. But the paper’s Discussion (page unavailable) says its EAE results implicate CCL20 in T-cell sensitization and exit from lymph nodes, rather than effector T-cell migration into the inflamed CNS. It therefore does not establish the claimed recruitment of pathogenic T cells to inflammatory sites. (LLM, conf=0.85)
Experimental — accuracy not yet measuredCCR6 and IL-23R have been linked to the pathogenicity of TH17 cells in autoimmune diseases.
“CCR6 and IL-23R have been linked to the pathogenicity of TH17 cells in autoimmune diseases (Hirota et al., 2007; Kohler et al., 2003; Langrish et al., 2005), such as multiple sclerosis, suggesting that the depression-associated hippocampal TH17 cells display CNS-directed pathogenic properties that may underlie a portion of their pro-depressive actions.”
From Distinct characteristics of hippocampal pathogenic th17 cells in a mouse model of depression (2018) · cites this paper as Kohler et al., 2003
The Discussion links CCL20, the ligand for CCR6, to the severity of experimental autoimmune encephalomyelitis, a T-cell-mediated model of CNS autoimmune inflammation. It does not identify the pathogenic T cells as TH17 cells or address IL-23R, and it locates CCL20’s demonstrated role in immune priming rather than the effector phase. (LLM, conf=0.86)
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Cites
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Surface phenotype and antigenic specificity of human interleukin 17–producing T helper memory cells
Acosta-Rodriguez, E. V., Rivino, L., Geginat, J., Jarrossay, D., Gattorno, M., Lanzavecchia, A., Sallusto, F., & Napolitani, G. (2007) · Nature Immunology · doi:10.1038/ni1467 · Cited by 1,828 · see citing works
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Distinct characteristics of hippocampal pathogenic th17 cells in a mouse model of depression
Beurel, E., Lowell, J. A., & Jope, R. S. (2018) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2018.04.012 · Cited by 65 · see citing works
- Authors
- Kohler, R. E., Caon, A. C., Willenborg, D. O., Clark-Lewis, I., & McColl, S. R.
- Affiliations
- The University of Adelaide (AU)
- Canberra Hospital (AU)
- Biomedical Research Center, University of British Columbia , Vancouver, British Columbia ,
- ORCID
- McColl, Shaun R
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2003-06
- Volume
- 170
- Issue
- 12
- Pages
- 6298-6306
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1540342549
- Cited by
- 79
- References
- 2
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 4 · 2017: 3 · 2016: 3 · 2015: 1 · 2014: 4 · 2013: 3 · 2012: 2
- FWCI
- 1.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Funders
- National Multiple Sclerosis Society
- Fordham University
- Multiple Sclerosis Society
- Medical Research Council
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- macrophage inflammatory protein-3α, CCL20, chemokines, experimental autoimmune encephalomyelitis, neuroinflammation, T cell-mediated inflammation, immune priming, lymphocyte sensitization, draining lymph nodes, neutralizing antibodies, adoptive transfer, central nervous system
- MeSH terms
- Animals, Cell Migration Inhibition, Cell Movement, Cells, Cultured, Encephalomyelitis, Autoimmune, Experimental, Female, Immune Sera, Immunization, Lymph Nodes, Mice, Inbred BALB C, Mice, Inbred Strains, Spinal Cord, T-Lymphocytes, Up-Regulation, Disease Progression, Myelin Proteolipid Protein, Macrophage Inflammatory Proteins, Receptors, Chemokine, Chemokines, CC, Mice, Receptors, CCR6, Chemokine CCL20
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