Therapeutic targets of misguided T cells in systemic lupus erythematosus

Tsutomu Takeuchi, Kensei Tsuzaka, Hideto Kameda, Kouichi Amano

Research output: Contribution to journalReview article

5 Citations (Scopus)

Abstract

It is widely accepted that T cells with defective function play a central role in the pathogenesis of systemic lupus erythematosus (SLE). The detailed molecular mechanism underlying the aberrant function of SLE T cells is now being revealed. The TCR zeta chain, transcription factor, elf-1, inflammation signal transducer NF-kB, and PKC theta have been identified as the responsible molecules. In contrast to the defective signal transduction molecules, surface structures such as adhesion molecules, and co-stimulators have been reported to increase in their expression and function. Glucocorticoids and immunosuppressive agents have greatly improved the outcome of acute diseases and 5-year survival rate. However, it is suggested that long-term survival and quality of life appears to be unsatisfactory. Although the medical management of SLE is not sufficient to warrant long-term survival of young patients, recent progress in anti-cytokine biologics therapy against rheumatoid arthritis (RA) has facilitated searching for the molecular targets of SLE. In this report, we briefly review the molecular basis of SLE pathogenesis, and discuss possible therapeutic targets in this disease, focusing particularly on signal transduction and adhesion molecules in T cells.

Original languageEnglish
Pages (from-to)295-298
Number of pages4
JournalCurrent Drug Targets: Inflammation and Allergy
Volume4
Issue number3
DOIs
Publication statusPublished - 2005 Jun 1
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pharmacology

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