EL PASO, Texas – Charlotte M. Vines, Ph.D., at The University of Texas at El Paso, has been awarded a $1.51 million grant to study how the C-C chemokine receptor type 7 (CCR7) regulates the levels of antibodies made during a secondary immune response.
The National Institutes of Health (NIH) National Institute of General Medical Sciences awarded the grant to Vines, an assistant professor of biological sciences. She will examine CCR7’s role in controlling the numbers and types of antibodies produced when a person or animal’s body detects a foreign substance (also known as an antigen) again in the future.
“This research has applications everywhere,” Vines said. “We’re trying to understand how the absence of CCR7 leads to an enhanced immune response.”
CCR7 is a receptor – a protein molecule within the plasma membrane of a cell – that sends the cells on which the receptor is found into the lymph nodes. In particular, the ligands (ions or neutral molecules) for CCR7 are chemokines, which means they are signaling proteins secreted by cells that make cells with CCR7 on their surface travel to lymph nodes. This is one reason why lymph nodes swell when a host’s body recognizes an antigen.
By studying the role of CCR7 within the immune system’s secondary response, Vines plans to expand on research findings that showed current theories regarding the immune system response to antigens do not align with how the immune system actually responds.
Imagine CCR7 as a light switch and the cell as a room. When the light switch is on (when CCR7 is active), the immune system response is controlled and measured. Conventional theories about the immune response are that if the light switch is off (CCR7 is absent or deactivated), the immune system shouldn’t respond because it doesn’t know the cell needs anything done.
Preliminary research has shown this to be incorrect. When CCR7 is not present, the immune system response is delayed, but the immune system’s creation of antibodies to fight off antigens dramatically increases. It appears as though the job of the CCR7 receptor is to dampen the immune response – and Vines and her team hope to discover why that happens and how being able to turn off or block that receptor might lead to new ways of treating diseases or illnesses using the secondary immune response.
Vines and her team of researchers plan to spend the next four years learning why more immune system activity happens when CCR7 is absent than when it is present. Research has shown that people who do not properly regulate CCR7 have autoimmune diseases like Hashimoto’s thyroiditis, Lupus and Sjogren’s syndrome.
Understanding what happens in the absence of CCR7 and the subsequent enhanced immune response has many applications in medicine.
For example, by uncovering what happens when inducing an autoimmune response by turning off a chemokine receptor like CCR7 could lead to future medical treatments in using a patient’s own immune system to fight off a disease or infection that does not have a well-developed vaccine for it such as the Ebola virus or HIV.
There also are possible cancer-fighting applications. By understanding how to turn off these receptors with an antagonist (think of an antagonist as someone going to that room, flipping the switch off and covering the light switch with duct tape), one day a treatment could be created where an antigen is introduced alongside the antagonist and the body would be able to fight off the tumor on its own by using its natural autoimmune response.