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Updated: May 7, 2026
Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
Single-cell transcriptome reveals highly complement activated microglia cells in association with pediatric
Siwei Mo1,2, Chenyan Shi2,3, Yi Cai2
1Department of Respiratory Medicine, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing Key Laboratory of Pediatrics, Chongqing, China.
Tuberculous meningitis (TBM) involves immune dysregulation. Microglial Macro_C01 cells activate complement and recruit CD4_C04 cells, amplifying inflammation in TBM.
Area of Science:
- Immunology
- Neuroscience
- Infectious Diseases
Background:
- Tuberculous meningitis (TBM) is a severe form of tuberculosis (TB) with high mortality and disability.
- The precise immune mechanisms driving TBM pathogenesis remain unclear.
Purpose of the Study:
- To elucidate the immune cell populations and interactions involved in TBM pathogenesis.
- To identify key cellular players and molecular pathways contributing to neuroinflammation in TBM.
Main Methods:
- Single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) and cerebrospinal fluid (CSF) cells from children with TBM.
- Unsupervised clustering, gene expression profiling, and ELISA validation of proteins and cytokines.
Main Results:
- Identified 33 distinct monocyte populations in PBMCs and CSF.
- Discovered enrichment of CD4_C04 (Th17/Th1) and Macro_C01 (microglia) cells in CSF.
- Macro_C01 cells, activated by complement, were linked to neuroinflammation and recruitment of CD4_C04 cells via CXCL16/CXCR6, with elevated inflammatory markers in CSF.
Conclusions:
- Microglial Macro_C01 cells activate complement and interact with CD4_C04 cells, amplifying inflammatory signals in TBM.
- This interaction may drive hyperinflammation and the immune response to *Mycobacterium tuberculosis* infection in the central nervous system.
