Abstract
T cells in SLE patients are dysfunctional as a result of altered signalling inputs and altered signal processing. They contribute to pathogenesis through expansion of autoreactive T cells, aberrant B-cell help and direct T cell-mediated tissue damage. Tissue inflammation and damage, in turn, produce nuclear autoantigens and perpetuate antigen presentation to T cells. Improvements in T cell-targeted therapy will require biomarkers of T-cell dysfunction that predict clinical response. Criteria for defining such biomarkers in SLE are discussed here. Phenotypes associated with T-cell activation, specific effector functions, and/or altered proliferative and homeostatic dynamics are promising candidates.
Keywords: Biomarker, T-cell activation, T-cell signalling, systemic lupus erythematosus, autoimmunity, immunodeficiency, proliferation, lymphopenia, effector function
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