Leading the way to a cure


Dissecting a Novel Molecular Genetic B-Cell Pathway in Lupus

Alarcón-Riquelme, Marta E., MD, PhD

Oklahoma Medical Research Foundation

Dr. Alarcon-Riquelme and her team have identified several lupus susceptibility genes, genes that make people more likely to develop lupus. However, they do not know how these genes lead to the development of the disease. 

With this grant, the researchers will focus on two genes, BANK1 and BLK. Their own data suggests these genes may play a role in the toll-like receptor (TLR) pathway, a critical signaling pathway with which cells communicate with each other. Previous research found that this pathway is very important in the development of lupus, triggering the production of autoantibodies and highly inflammatory substances such as alpha-interferon that underlie the disease process. Up to 70 percent of all people with lupus produce too much alpha-interferon. 

The researchers want to better understand the role of these two genes in the TLR9 pathway. As part of their investigation, they will work with human cell lines that do not express these genes. This will enable them to see if the lack of genetic expression changes the ability of cells in the TLR9 pathway to respond and produce inflammatory chemicals. 

They will also use an animal model that does not express the genes so they can test the effects of certain stimuli on the animals’ immune systems. The researchers will also see if deleting one or both genes leads to the development of autoantibodies or kidney inflammation, and how that development occurs.

What this study means for people with lupus: The results of this research will increase our knowledge of the rule of susceptibility genes in the development of lupus, enabling the construction of models and systems for testing potential therapeutic substances that could affect the underlying cause of the disease, not just its symptoms.

1.5 million

people in the U.S. have Lupus.

172 million

dollars committed to lupus research by the Lupus Research Alliance.

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