Astrocytes express functional chemokine receptors
M E Dorf1, M A Berman, S Tanabe
1Department of Pathology, Harvard Medical School, 02115, Boston, MA, USA. dorf@hms.harvard.edu
Chemokine receptors on astrocytes, like CXCR4 and CCR5, are expressed at low levels but can increase during disease. This suggests chemokines play a broader role in regulating central nervous system inflammation.
Area of Science:
- Neuroimmunology
- Cellular and Molecular Neuroscience
Background:
- Astrocytes, crucial glial cells in the central nervous system (CNS), play roles in neuroinflammation.
- Chemokines are signaling proteins that regulate immune cell trafficking and function.
- The expression and function of chemokine receptors on astrocytes are not fully elucidated.
Purpose of the Study:
- To characterize the functional expression of various chemokine receptors on astrocytes.
- To investigate the potential role of astrocytes in chemokine-mediated inflammatory responses within the CNS.
Main Methods:
- Analysis of multiple lines of evidence to identify chemokine receptor expression on astrocytes.
- Investigation of receptor expression levels under basal conditions, during disease, and following cytokine induction.
Main Results:
- Functional expression of chemokine receptors CXCR4, CCR1, CCR5, and CX3CR1 was identified on astrocytes.
- These receptors are typically expressed at low levels, but expression can be upregulated in disease or by cytokines.
- Evidence suggests the expression of additional receptors, including CXCR2, CCR2, and others linked to HIV-1 infection.
- Chemokines can induce further chemokine synthesis in astrocytes, amplifying CNS inflammatory responses.
Conclusions:
- Astrocytes express a range of functional chemokine receptors, indicating a significant role in CNS immune regulation.
- The ability of astrocytes to synthesize chemokines suggests a mechanism for amplifying inflammatory responses in the central nervous system.
- These findings highlight the broader involvement of chemokines in regulating CNS functions and neuroinflammation.
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