Defensins in systemic lupus erythematosus

Oren Froy*, Zev M. Sthoeger

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

20 Scopus citations


Systemic lupus erythematosus (SLE) is an autoimmune disease, resulting in inflammation and tissue damage. The precise etiology for SLE is so far unknown. It has been shown that the innate immunity plays a role in SLE pathogenesis. The innate immune system confers broad protection against pathogens by the secretion of broad-spectrum antibacterial and immunomodulatory substances named defensins. Recently, α-defensin, the products of neutrophils have been found to be upregulated at the mRNA and protein levels in SLE patients. In addition, increased antidefensin antibodies were found in sera of patients with SLE, but these levels decreased after therapy with corticosteroids. These recent findings suggest a role for defensins in the pathogenesis of SLE. Thus, activation and degranulation of neutrophils leads to α-defensin secretion in SLE patients. Given their immunomodulatory role, α-defensin secretion might activate the adaptive immune system leading to the stimulation of the immune system, as is manifested in SLE.

Original languageAmerican English
Title of host publicationContemporary Challenges in Autoimmunity
PublisherBlackwell Publishing Inc.
Number of pages5
ISBN (Print)9781573317627
StatePublished - Sep 2009

Publication series

NameAnnals of the New York Academy of Sciences
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632


  • Defensin
  • Human neutrophil peptide
  • Systemic lupus erythematosus


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