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Review
. 2008 Jan;7(3):256-61.
doi: 10.1016/j.autrev.2007.11.020. Epub 2007 Dec 4.

Novel molecular targets in the treatment of systemic lupus erythematosus

José C Crispín  1 , George C Tsokos
Affiliations
Review

Novel molecular targets in the treatment of systemic lupus erythematosus

José C Crispín et al. Autoimmun Rev. 2008 Jan.

Abstract

T cells from patients with systemic lupus erythematosus (SLE) display a number of biochemical abnormalities which include altered expression of key signaling molecules, heightened calcium responses, and skewed expression of transcription factors. These defects are involved in the altered behavior of SLE T cells and are probably central in the disease pathogenesis. The aim of this communication is to review the defects that have been consistently documented in SLE T cells, highlighting molecules and pathways that represent therapeutic targets.

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Figures

Figure 1
Figure 1. The biochemical defects of SLE T cells translate into specific phenotypic characteristics
The decrease in CD3ζ levels and its substitution by FcRγ-Syk leads to increased calcium response upon TCR stimulation. The former has a number of downstream consequences including altered gene expression (A). Increased ERM phosphorylation by Rho kinase (ROCK) leads to lipid raft clustering and augmented CD44-mediated T cell adhesion and migration.
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References

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