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Abstract
ABSTRACT Multiple sclerosis (MS) is a chronic autoimmune disease of the CNS characterized by inflammation, demyelination, and axonal injury. These pathologic effects are manifested in clinical symptoms of relapse and disability. Various disease-modifying therapies have been developed in recent years to modulate the body's immune response. Among the most widely used are the beta interferons (IFNβ). All produce comparable biological effects and are approved for the treatment of relapsing-remitting MS (RRMS). Although the precise mechanisms through which IFNβ achieves its antiinflammatory and immunomodulatory effects remain uncertain, several modes of action have been proposed, including inhibition of T-cell activation and proliferation; apoptosis of autoreactive T cells; induction of regulatory T cells; inhibition of leukocyte migration across the blood-brain barrier; cytokine modulation; and potential antiviral activity. Endogenously produced IFNβ in the injured brain is also now believed to contribute to mediation of antiinflammatory and regenerative effects. All these mechanisms are believed to underlie the therapeutic effect of IFNβ in the treatment of RRMS.
Glossary
- APC=
- antigen-presenting cells;
- BAFF=
- B-cell-activating factor;
- BBB=
- blood-brain barrier;
- EAE=
- experimental autoimmune encephalitis;
- Gd=
- gadolinium;
- IFN=
- interferon;
- IFNAR=
- type 1 IFN receptor;
- IL=
- interleukin;
- MHC=
- major histocompatibility complex;
- MMP=
- matrix metalloproteinase;
- MS=
- multiple sclerosis;
- PBMC=
- peripheral blood mononuclear cells;
- PD1−=
- programmed death receptor 1-negative;
- RRMS=
- relapsing-remitting multiple sclerosis;
- SC=
- subcutaneous;
- SLE=
- systemic lupus erythematosus;
- sTNF-RII=
- soluble TNF-receptor II;
- sVCAM=
- soluble vascular cell adhesion molecule-1;
- TGF=
- transforming growth factor;
- Th=
- T helper;
- TIMP-1=
- tissue inhibitor of MMP-type 1;
- TNF=
- tumor necrosis factor;
- Treg=
- T regulatory;
- TRIF=
- Toll-IL-1 receptor domain-containing adaptor inducing IFNβ;
- VLA-4=
- very late antigen-4.
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