​​​​​​​News of Note—Understanding Lyme arthritis; expanding J&J’s cancer drug Imbruvica; a key gene mutation in inflammatory disease

tick on a leaf
The tick-borne Lyme disease can cause persistent arthritis. University of Utah researchers have identified a protein that might kick off that inflammatory process. (Wikimedia Commons)

How a tick bite causes Lyme arthritis

Some of the 300,000 Americans who contract Lyme disease from a tick bite each year develop persistent arthritis, even after antibiotics clear the bacteria. Researchers at University of Utah Health believe they have figured out why that happens. They identified a protein receptor on the surface of the immune system’s T cells that interacts with molecules on Borrelia burgdorferi, the bacteria that causes Lyme. This interaction prompts T cells to produce inflammatory molecules, which in turn build up around joints, causing pain. The discovery may point to new therapies to target this inflammation, they suggest. The research was published in the Journal of Immunology. (Release)

A new use for an old cancer drug?

Johnson & Johnson’s Imbruvica (ibrutinib), a Bruton’s tyrosine kinase inhibitor, was approved to treat leukemia in 2013, and now researchers at Arizona State University believe they have found a new use for the drug. They have discovered that Imbruvica also inhibits ERBB4, another tyrosine kinase that’s believed to contribute to the growth and progression of cancer. Irregularities in ERBB4 have been implicated in many types of cancer, including melanoma, neuroblastoma and colon cancer, raising the prospect of expanding the role of ibrutinib in oncology, they suggest in the journal Oncogene. The team made the discovery using a screening method they developed that specifically searches for new targets for existing drugs. The technology is a microarray that can simultaneously examine the interactions of many different proteins. (Release)

A key gene mutation in inflammatory disease

Researchers at Cincinnati Children’s Hospital Medical Center have discovered that a mutation in the gene Gimap5 promotes immune disorders by affecting T cell functioning. They made the discovery by studying immune cells donated by a 16-year-old boy with lymphopenia, a deficiency of white blood cells. When Gimap5 is working properly, it regulates a protein that inactivates the enzyme GSK3. That process is important to preserving the lives of T cells. The Cincinnati Children’s team discovered that drugs designed to inhibit GSK3 improve immune functioning in mice and restore T cell functioning in human cells, they explained in the journal Nature Communications. They are studying the potential of GSK3 inhibitors in lupus and allergic lung disease. (Release)


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