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T cells in amyotrophic lateral sclerosis
Author(s) -
Holmøy T.
Publication year - 2008
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.2008.02065.x
Subject(s) - amyotrophic lateral sclerosis , neuroscience , neuroinflammation , microglia , motor neuron , neuroprotection , neurodegeneration , medicine , glatiramer acetate , neurogenesis , t cell , spinal cord , multiple sclerosis , inflammation , immune system , immunology , biology , disease , pathology
The inflammatory process in ALS involves infiltration of T cells and activation of antigen presenting cells co‐localizing with motor neuron damage in the brain and spinal cord. The role of T cells in the pathogenic process is not settled. T cells may damage motor neurons by cell‐cell contact or cytokine secretion, or contribute indirectly to motor neuron damage through activation of microglia and macrophages. Alternatively, T cell infiltration may be an epiphenomenon related to clearance of dead motor neurons. Lessons from animal models of neuroinflammation and neurodegeneration have shown that T cell responses can be neuroprotective or even enhance neurogenesis. Therefore, it is possible that T cells can be induced to slow motor neuron destruction and facilitate repair in ALS. The T cell modulating drug glatiramer acetate has shown promising results in animal models, and is being currently investigated in a phase II trial in ALS. This paper reviews the evidence for T cells as pathogenic players and therapeutic targets in ALS.