Related Experiment Video
Updated: Feb 25, 2026
An In Vitro Model for the Study of Cellular Pathophysiology in Globoid Cell Leukodystrophy
Published on: October 21, 2014
Microglia activation induced by serum of SLE patients
Jianing Wang1, Chunshu Yang2, Qi Zhao1
1Department of Rheumatology and Immunology, First Affiliated Hospital, China Medical University, Shenyang 110001, People's Republic of China.
Abstract:
To investigate the potential involvement of microglia in the neuropathology of systemic lupus erythematosus (SLE), we examined whether SLE patient sera could activate BV2 microglia in vitro. Exposure to SLE patient sera resulted in morphological changes in the microglia, an increase in MHC II and CD86 protein expression, and an obvious release of nitric oxide and proinflammatory cytokines. However, the SLE sera did not induce a specific change in the production of immunoregulatory cytokines. Inactivating complements or neutralizing proinflammatory cytokines in the SLE sera did not suppress microglial activation. Our results highlight the potential role of microglia in neuroinflammation in SLE patients.
Insights
Systemic lupus erythematosus (SLE) patient sera activate microglia, increasing pro-inflammatory markers and nitric oxide. This suggests microglia play a role in neuroinflammation associated with SLE, even without complement or cytokine neutralization.
Area of Science:
- Neuroimmunology
- Rheumatology
Background:
- Systemic lupus erythematosus (SLE) is an autoimmune disease that can affect the central nervous system.
- The role of microglia, the brain's resident immune cells, in SLE neuropathology is not fully understood.
Purpose of the Study:
- To investigate the potential involvement of microglia in SLE neuropathology.
- To determine if sera from SLE patients can activate microglia in vitro.
Main Methods:
- BV2 microglia were exposed to sera from SLE patients in vitro.
- Microglial activation was assessed by morphological changes, protein expression (MHC II, CD86), nitric oxide release, and cytokine production.
- Experiments included complement inactivation and pro-inflammatory cytokine neutralization in SLE sera.
Main Results:
- SLE patient sera induced morphological changes in microglia.
- Exposure to SLE sera increased MHC II and CD86 protein expression, nitric oxide, and pro-inflammatory cytokine release.
- Neither complement inactivation nor pro-inflammatory cytokine neutralization suppressed microglial activation by SLE sera.
- No specific change in immunoregulatory cytokine production was observed.
Conclusions:
- Microglia are activated by SLE patient sera in vitro.
- Microglial activation involves increased pro-inflammatory mediators and nitric oxide.
- These findings suggest a potential role for microglia in neuroinflammation within SLE patients.
