Michael C. Schneider, MD
Southern Illinois University School of Medicine, Springfield, IL
The blood of people with lupus characteristically contains antibodies to DNA, our genetic material. DNA-associated factors and deposits of complexes of antibodies, plus DNA in tissues and organs, are believed to cause a number of lupus symptoms.
The body has a number of ways to degrade DNA released from cells that normally age and die, including several types of proteins called DNASEs.
Given that a deficiency of one of the DNASEs that may cause lupus was proposed more than 40 years ago, Dr. Schneider set out with LRI funding in 2002 to establish whether an enzyme that can destroy DNA released by dying cells-DNASE1-like 3-might help prevent autoimmunity and lupus-like disease.
He tested the hypothesis in mouse models of lupus. Would a deficiency in the DNASE1-like 3 protein provide protection from the genetic alteration of cells by DNA that contributes to the development of lupus?
His findings, published in the Journal of Clinical and Experimental Immunology, reveal that two lupus-prone mouse strains that carry mutations in the DNASE1-like3 gene do mildly impair its activity.
“Work funded by the LRI is really innovative compared to other organizations.” – Michael Schneider, MD
Dnase1l3 deficiency in lupus-prone MRL and NZB/W F1 mice. Clin Exp Immunol. 2003 Oct;134(1):46-52. Wilber A, O'Connor TP, Lu ML, Karimi A, Schneider MC.
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- B Cells
- Cardiovascular System
- Cell Signaling
- Central Nervous System
- Dendritic Cells
- Environmental Triggers
- Gender Matters
- General Immune System Function
- Human Lupus Biology
- Lupus Pregnancy
- New to Lupus
- New Treatments
- T Cells
- Target Identification
- Why the Lupus Immune System Reacts to Its Own DNA