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Abstract
Once perceived as a region of limited immune activity, the CNS is now known to be an important site of immune interactions. Activated T cells can infiltrate the blood-brain barrier where they accumulate and proliferate in response to antigen restimulation. These leukocytes express proinflammatory cytokines that help in activating microglia and other immune cells. A profound inflammatory response ensues, which can lead to axonal injury and demyelination. In contrast, other T cells can be neuroprotective. CD4+ Th2 cells secrete anti-inflammatory cytokines and can elicit the production of bioactive neurotrophins from CNS glia. In addition, neurons themselves can contribute to immune system regulation by being targets of neurotoxic T cells or by altering T-cell activity, including the generation of regulatory T cells. The interplay between components of the immune system and CNS contributes both to healthy brain function and to the pathogenesis of neurodegenerative diseases such as multiple sclerosis.
Glossary
- ARD=
- autoimmune rheumatic diseases;
- BBB=
- blood-brain barrier;
- BDNF=
- brain-derived neurotrophic factor;
- EAE=
- experimental autoimmune encephalitis;
- ECM=
- extracellular matrix;
- FGF=
- fibroblast growth factor;
- HPA=
- hypothalamic-pituitary-adrenal;
- IGF=
- insulin-like growth factor;
- IL=
- interleukin;
- IVIG=
- IV immunoglobulin;
- SCI=
- spinal cord injury;
- MHC=
- major histocompatibility complex;
- MMP=
- matrix metalloproteinase;
- M/M=
- monocytes/macrophages;
- NT-3=
- neurotrophin-3;
- NO=
- nitric oxide;
- OPC=
- oligodendrocyte precursor cell;
- PDGF=
- platelet-derived growth factor;
- TLR=
- toll-like receptor;
- TNF=
- tumor necrosis factor.
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