Elkon LabDr. Keith Elkon's research objective is to better define the molecular and genetic basis for autoimmune diseases such as lupus and arthritis. There is a major unmet medical need in lupus. There has been only one new drug approved by the FDA in the last 50 years and the drugs in common use today have significant side effects. Therefore there is a pressing need both to better understand how the disease develops and to use that knowledge to devise new, more effective forms of therapy in lupus and related diseases.

Type I Interferons

Type I interferons are the major inflammatory proteins made by the innate immune system following virus infections. Surprisingly overexpression of type I interferon is very prominent feature observed in about three quarters of Lupus (SLE) patients as well as in related autoimmune diseases such as scleroderma, polymyositis and primary Sjogren’s syndrome. There is also some suggestion that this pathway may be implicated in organ specific autoimmune diseases such as Type 1 Diabetes and some cases of rheumatoid arthritis. Nucleic acids from dying cells are strongly implicated in stimulating interferon in autoimmune diseases. 

Major Goals of Research

The two major goals of Dr. Elkon’s research are to understand the abnormalities in the innate immune system responsible for initiating the autoimmune diseases such as lupus and to use this knowledge to design new forms of therapy that could work on the earliest stages of disease to prevent severe inflammation.

Current research projects address the following questions:

  • What are the cell death abnormalities that provoke an immune response?
  • How does the cell debris released from dying cells stimulate inflammation - especially the type 1 interferon response?
  • Which interferon pathways are specifically abnormal in lupus and related autoimmune disorders?
  • Can environmental triggers such as sunlight be used to uncover differences in the interferon response in lupus versus controls?
  • How can rheumatologists develop therapeutics to abrogate early activation of interferon pathways?