Neuroinflammation in multiple sclerosis: evidence for autoimmune dysregulation, not simple autoimmune reaction.
Both inflammatory and neurodegenerative components may contribute to the clinical profile of multiple sclerosis (MS) leading to irreversible deficits when they exceed the threshold of compensation. The mechanisms leading to tissue injury in MS are complex. Inflammation appears to be caused by overactive pro-inflammatory T-helper 1 cells, initiating an inflammatory cascade with several cellular and molecular immune components participating in the pathogenetic mechanism. Current treatments are most effective in the inflammatory phase of the disease since they may interfere with various stages of the immune cascade. Recent evidence has emerged that inflammation may not only be destructive, but may also play a part in tissue repair. This has opened up a new aspect of our knowledge of the role of the inflammatory process in MS. Data regarding the role of regulatory cells in particular, imply that specific immunomodulatory strategies that support the function of these particular cellular subpopulations may participate in the downregulation of autoimmune responses in MS.
Grigoriadis
Nikolaos
N
Department of Neurology, Laboratory of Experimental Neurology and Neuroimmunology, AHEPA University Hospital, Aristotle University of Thessaloniki, 1 Stilp Kyriakidi str 54636, Thessaloniki, Greece. grigoria@med.auth.gr
Grigoriadis
Savas
S
Polyzoidou
Eleni
E
Milonas
Ioannis
I
Karussis
Dimitrios
D
D015551:Autoimmunity / Q000502:physiology*; D051858:Forkhead Transcription Factors / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D009103:Multiple Sclerosis / Q000276:immunology* / Q000473:pathology* / Q000503:physiopathology; D050378:T-Lymphocytes, Regulatory / Q000502:physiology
C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors