JAK2 inhibition in murine systemic lupus erythematosus

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Systemic lupus erythematosus is a systemic autoimmune disease characterized by the presence of myriad autoantibodies, some with pathogenic potential, and diverse clinical manifestations. Involvement of the kidney is a major cause of morbidity and mortality in human lupus patients and in murine models of the disease. It is hoped that more specific inhibition of crucial disease pathways would improve patient response rates, while reducing the considerable rates of drug-related side effects associated with current therapy. IL-6 has a pivotal regulatory role in the development and maturation of long-lived plasma cells, one of the key cell types driving the lupus disease phenotype as the source for the majority of lupus-related autoreactive antibodies. In this study, Lu et al. target the IL-6 signal transduction pathway using a specific JAK2 inhibitor of the JAK-STAT pathway, CEP-33779. In murine lupus models, they show significant improvement in nephritis, and prolonged survival, in mice treated with CEP-33779. The study presents the promise of a novel pathway for therapeutic intervention in systemic lupus erythematosus using a medication administered orally.

Original languageEnglish (US)
Pages (from-to)369-372
Number of pages4
JournalImmunotherapy
Volume4
Issue number4
DOIs
StatePublished - Apr 2012

Fingerprint

Systemic Lupus Erythematosus
Interleukin-6
Nephritis
Plasma Cells
Drug-Related Side Effects and Adverse Reactions
Autoantibodies
Autoimmune Diseases
Signal Transduction
Morbidity
Phenotype
Kidney
Survival
Mortality
Antibodies
Therapeutics
CEP 33779

Keywords

  • IL-6
  • JAK-2
  • lupus nephritis
  • plasma cells
  • SLE

ASJC Scopus subject areas

  • Immunology and Allergy
  • Oncology
  • Immunology

Cite this

JAK2 inhibition in murine systemic lupus erythematosus. / Tagoe, Clement E.; Putterman, Chaim.

In: Immunotherapy, Vol. 4, No. 4, 04.2012, p. 369-372.

Research output: Contribution to journalArticle

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