Cytokines, chemokines, and cytokine receptors in human microglia
Abstract
Enriched populations of human microglial cells were isolated from mixed cell cultures prepared from embryonic human telencephalon tissues. Human microglial cells exhibited cell type-specific antigens for macrophage-microglia lineage cells including CD11b (Mac-1), CD68, B7-2 (CD86), HLA-ABC, HLA-DR and ricinus communis aggulutinin lectin-1 (RCA-1), and actively phagocytosed latex beads. Gene expression and protein production of cytokines, chemokines and cytokine/chemokine receptors were investigated in the purified populations of human microglia. Normal unstimulated human microglia expressed constitutively mRNA transcripts for interleukin- 1beta (IL-1beta) -6, -8, -10, -12, -15, tumor necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and monocyte chemoattractant protein-1 (MCP-1), while treatment with lipopolysaccharide (LPS) or amyloid beta peptides (Abeta) led to increased expression of mRNA levels of IL-8, IL-10, IL-12, TNF-alpha, MIP-1alpha, MIP-1beta, and MCP-1. Human microglia, in addition, expressed mRNA transcripts for IL-1RI, IL-1RII, IL-5R, IL-6R, IL-8R, IL-9R, IL-10R, IL-12R, IL-13R, and IL-15R. Enzyme-linked immunosorbent assays (ELISA) showed increased protein levels in culture media of IL-1beta, IL-8, TNF-alpha, and MIP-1alpha in human microglia following treatment with LPS or Abeta. Increased TNF-alpha release from human microglia following LPS treatment was completely inhibited with IL-10 pretreatment, but not wi…
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Within the brain, major histocompatibility complex II is primarily expressed on microglia, where it is generally considered a marker of activated cells, though it may have weaker expression in resting cells.
“Within the brain, MHCII is primarily expressed on microglia, where it is generally considered a marker of activated cells, though it may have weaker expression in resting cells.14”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [14]
CD68 labels the lysosome and is commonly considered a marker of activated phagocytic microglia.
“Although there is some CD68 expression on resting microglia,14 it labels the lysosome and is therefore commonly considered a marker of activated phagocytic microglia.60”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [14]
CD11b is expressed by both resting and activated microglia, though it is inducible with activation.
“Like Iba1, CD11b is expressed by both resting and activated microglia, though it too is inducible with activation.14”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [14]
Cites
Perivascular microglial cells of the CNS are bone marrow-derived and present antigen in vivo
Hickey, W. F., & Kimura, H. (1988) · Science · doi:10.1126/science.3276004 · Cited by 1,466 · see citing works
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Inflammation as a central mechanism in Alzheimer's disease
Kinney, J. W., Bemiller, S. M., Murtishaw, A. S., Leisgang, A. M., Salazar, A. M., & Lamb, B. T. (2018) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2018.06.014 · Cited by 2,253 · see citing works
The pivotal link between ACE2 deficiency and SARS-CoV-2 infection
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“[26,27] It is important to remark that the deleterious effects of angiotensin II summarized above almost entirely result from the stimulation of AT1 receptors.”
The role of inflammation in Alzheimer’s disease
Tuppo, E. E., & Arias, H. R. (2005) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2004.07.009 · Cited by 734 · see citing works
Gupta, N., Brown, K. E., & Milam, A. H. (2003) · Experimental Eye Research · doi:10.1016/s0014-4835(02)00332-9 · Cited by 582 · see citing works
Hopperton, K. E., Mohammad, D., Trépanier, M. O., Giuliano, V, & Bazinet, R. P. (2018) · Molecular Psychiatry · doi:10.1038/mp.2017.246 · Cited by 567 · see citing works
The role of interleukin-6 signaling in nervous tissue
Rothaug, M., Becker-Pauly, C., & Rose-John, S. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2016.03.018 · Cited by 491 · see citing works
Innate immunity and inflammation in ageing: a key for understanding age-related diseases
Licastro, F., Candore, G., Lio, D., Porcellini, E., Colonna-Romano, G., Franceschi, C., & Caruso, C. (2005) · Immunity & Ageing · doi:10.1186/1742-4933-2-8 · Cited by 453 · see citing works
Neuroinflammatory processes in Alzheimer’s disease
Heneka, M. T., O’Banion, M. K., Terwel, D., & Kummer, M. P. (2010) · Journal of Neural Transmission · doi:10.1007/s00702-010-0438-z · Cited by 433 · see citing works
Wilkinson, M. B., Xiao, G., Kumar, A., LaPlant, Q., Renthal, W., Sikder, D., Kodadek, T. J., & Nestler, E. J. (2009) · Journal of Neuroscience · doi:10.1523/jneurosci.0932-09.2009 · Cited by 262 · see citing works
Antidepressant therapies inhibit inflammation and microglial M1-polarization
Kalkman, H. O., & Feuerbach, D. (2016) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2016.04.001 · Cited by 212 · see citing works
Mutant α-Synuclein Overexpression Mediates Early Proinflammatory Activity
Su, X., Federoff, H. J., & Maguire-Zeiss, K. A. (2009) · Neurotoxicity Research · doi:10.1007/s12640-009-9053-x · Cited by 145 · see citing works
Paglinawan, R., Malipiero, U., Schlapbach, R., Frei, K., Reith, W., & Fontana, A. (2003) · Glia · doi:10.1002/glia.10286 · Cited by 122 · see citing works
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Laffer, B., Bauer, D., Wasmuth, S., Busch, M., Jalilvand, T. V., Thanos, S., Meyer zu Hörste, G., Loser, K., Langmann, T., Heiligenhaus, A., et al. (2019) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2019.00430 · Cited by 120 · see citing works
Gut microbiota–driven brain Aβ amyloidosis in mice requires microglia
Dodiya, H. B., Lutz, H. L., Weigle, I. Q., Patel, P., Michalkiewicz, J., Roman-Santiago, C. J., Zhang, C. M., Liang, Y., Srinath, A., Zhang, X., et al. (2022) · Journal of Experimental Medicine · doi:10.1084/jem.20200895 · Cited by 120 · see citing works
Rentzos, M., Zoga, M., Paraskevas, G. P., Kapaki, E., Rombos, A., Nikolaou, C., Tsoutsou, A., & Vassilopoulos, D. (2006) · Journal of Geriatric Psychiatry and Neurology · doi:10.1177/0891988706286226 · Cited by 65 · see citing works
The role of soluble intercellular adhesion molecules in neurodegenerative disorders
Rentzos, M., Michalopoulou, M., Nikolaou, C., Cambouri, C., Rombos, A., Dimitrakopoulos, A., & Vassilopoulos, D. (2005) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2004.11.001 · Cited by 45 · see citing works
Cytokine Signalling at the Microglial Penta-Partite Synapse
Aramideh, J. A., Vidal-Itriago, A., Morsch, M., & Graeber, M. B. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222413186 · Cited by 35 · see citing works
Ernest James Phillips, T., & Maguire, E. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.652593 · Cited by 33 · see citing works
- Authors
- Lee, Y. B., Nagai, A., & Kim, S. U.
- Affiliations
- University of British Columbia (CA)
- Corresponding author
- Kim, Seung U.
- Venue
- Journal of Neuroscience Research
- Publisher
- Wiley
- Published
- 2002-06-25
- Volume
- 69
- Issue
- 1
- Pages
- 94-103
- ISSN
- 0360-4012 (ISSN-L)
- 1097-4547
- OpenAlex
- W1984008481
- Cited by
- 363
- References
- 1
- Citations by year
- 2026: 11 · 2025: 8 · 2024: 12 · 2023: 18 · 2022: 14 · 2021: 16 · 2020: 18 · 2019: 24 · 2018: 8 · 2017: 8 · 2016: 14 · 2015: 9 · 2014: 16 · 2013: 18 · 2012: 15
- FWCI
- 11.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroscience Research (publishedVersion)
- PubMed (publishedVersion)
- AJOU Open Repository (Ajou University) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- cytokines, chemokines, cytokine receptors, IL-1β, TNF-α, MIP-1α, MCP-1, lipopolysaccharide, amyloid-beta, IL-10, microglial activation, neuroinflammation, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, stroke, neurotrauma
- MeSH terms
- Brain, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Humans, Cytokines, Microglia, Receptors, Cytokine, Gene Expression Regulation, Developmental, Chemokines, Reverse Transcriptase Polymerase Chain Reaction
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