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Microbial products induce autoimmune disease by an IL-12-dependent pathway
B M Segal1, D M Klinman, E M Shevach
1Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|June 1, 1997
Summary
Infections can trigger autoimmune diseases like experimental allergic encephalomyelitis (EAE). Microbial products induce interleukin-12 (IL-12), driving disease development by activating T cells.
Area of Science:
- Immunology
- Microbiology
- Neuroscience
Background:
- Autoimmune diseases are often preceded by infections.
- Microbial components like LPS and bacterial DNA can modulate cytokine production.
Purpose of the Study:
- To investigate the role of microbial products in autoimmune disease development.
- To identify the specific microbial factors and mechanisms driving experimental allergic encephalomyelitis (EAE).
Main Methods:
- Exposure of T cells to microbial products (LPS, bacterial DNA, CpG oligonucleotides).
- Assessment of T cell activation and cytokine production, specifically IL-12.
- Induction and transfer of EAE.
Main Results:
- Microbial products converted myelin basic protein-specific T cells into effector cells.
- These activated T cells were capable of transferring EAE.
- The disease-promoting effects of microbial products were dependent on IL-12 induction.
Conclusions:
- Microbial products can initiate and worsen autoimmune conditions.
- IL-12 production is a critical mediator linking microbial stimulation to autoimmune disease pathogenesis.
- Targeting IL-12 may offer a therapeutic strategy for autoimmune diseases.