Pol Merkuriusz Lek. 2003 Dec;15(90):570-3
Katedra i Klinika Neurologii AM we Wroclawiu.
Multiple Sclerosis is a T-cell mediated autoimmune disease leading to demyelination of central nervous system.
The precise mechanism by which auto-reactive T cells are activated and tolerance to self-antigens is broken are not fully understood.
The dysregulation of costimulatory signals between T cell and antigen presenting cell is taken into consideration in this process.
Among many costimulatory molecules presented on activated T cells CD40L and CD28 are of special interest.
These molecules are involved in the positive regulation of T cell activation.
Contrary to them CTLA-4, the another costimulatory molecule presented on activated T cells down-regulates activation.
In this review the role of modification of costimulatory signals on the development and course of EAE, the animal model for multiple sclerosis as well as clinical data documenting the dysregulation of costimulation in Multiple Sclerosis are presented.