About this Research Topic
The aberration of T cells in human SLE is well documented. Examples of this include; altered intracellular signaling network and epigenetic modification, deficiency and/or overproduction of cytokines and an imbalance in the subpopulations of T cells. These phenotypic irregularities could be potential therapeutic targets. Aberrant expression of syk and abnormal histone modification in lupus T cells could be a drug target. While deficiency of IL-2 production in lupus T cells could be involved in the pathogenesis of SLE, supplementation of low-dose IL-2 targeting Treg and/or Tfh would be a potential therapeutic strategy demonstrated both in human and in murine lupus. Accumulating evidence supports the notion that modulating T cell function could also prevent the progression of autoimmune-mediated tissue damage. For instance, targeting metabolism of T cells is a promising potential for SLE treatment. Inhibiting glycolysis of dysfunctional lupus T cells has been shown to ameliorate renal pathology as well as to reduce autoantibody titers in a mouse model. Further, inhibition of glutaminolysis of T cells resulted in the reduction of pathogenic Th17 cells in lupus.
This Research Topic aims to provide an update on the role of T cells in SLE. We welcome Reviews, Mini-reviews and Original Research articles for SLE with a clinical and/or experimental viewpoint focusing on, but not limited to:
1. T cell subpopulations in SLE including Tregs, Tfh, and CTLs
2. Cytokine dysregulation in SLE
3. Metabolic regulation of dysfunctional T cells
4. Epigenetic modifications in T Cells
Keywords: T cells, SLE, autoimmunity, immune tolerance
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