Protective autoimmunity is a condition in which cells of the adaptive immune system contribute to maintenance of the functional integrity of a tissue, or facilitate its repair following an insult.
Most of the studies on the phenomenon of protective autoimmunity were conducted in experimental settings of various CNS pathologies and thus reside within the scientific discipline of neuroimmunology.
The adaptive immune system primarily consists of T and B lymphocytes, which can respond to specific antigens and subsequently acquire an immunological memory.
Additional work by the Schwartz group has shown that protective autoimmunity is a naturally occurring physiological phenomenon that takes place spontaneously following a CNS injury.
Experiments conducted in animal models of spinal cord injury,[3][4] brain injury,[5] glaucoma,[6] stroke,[7][8] motor neuron degeneration,[9] Parkinson’s[10] and Alzheimer's disease[11][12] have demonstrated the relevance of immune cells and in particular T cells that recognize CNS antigens in promoting neuronal survival and functional recovery from acute and chronic neurodegenerative conditions.
[13][14] An immune response that takes place following CNS injury elicits a cascade of molecular and cellular events that can eventually affect the organism’s functional recovery.
[19] Experiments in animal models of CNS injury have shown that depletion of regulatory T cells allows an enhanced neuroprotective autoimmune response to take place after the insult.
Nevertheless, studies during the last decade have established that the immune system has the capacity to orchestrate a multitude of beneficial effects in the adult CNS under both normal and pathological conditions.
For therapeutic purposes, vaccination with an antigen associated with the site of injury (for example peptides derived from myelin proteins) is problematic, because it carries the risk of inducing, in individuals susceptible to autoimmune diseases, an overwhelming inflammatory response that is detrimental for recovery.
To circumvent this problem researchers have been using lower affinity agonists (termed ‘altered peptide ligands’) which induce a weaker immune response.
Experiments in animal models of spinal cord injury revealed that the use of such altered peptide ligands is effective in promoting functional recovery without the risk of inducing a deleterious autoimmune response.