T cells in Systemic Lupus Erythematosus

• T cell transcriptomes can stratify patients.
• TH17, Double-Negative and γδT cells contribute to lupus nephritis.
• T cell support autoantibody production in lymphoid and non-lymphoid organs in SLE.
• Aberrant activation of several pathways drives T cell malfunction in SLE.
• CaMKIV, ROCK, STAT3 AND PI3K/AKT/mTOR represent therapeutic targets.

Systemic Lupus Erythematosus is an autoimmune disorder caused by a complex combination of genetic, epigenetic and environmental factors. Different polymorphisms and epigenetic modifications lead to altered gene expression and function of several molecules which lead to abnormal T cell responses. Metabolic and functional alterations result in peripheral tolerance failures and biased differentiation of T cells into pro-inflammatory and B cell-helper phenotypes as well as the accumulation of disease-promoting memory T cells. Understanding these T cell alterations and their origins is necessary to develop more accurate patient classification systems and to discover new therapeutic targets.

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