Success of Antiviral Immune Response Depends on Interleukin-21

Results from a recent study on the immune response to viral infection in a mouse model emphasized the critical role of interleukin-21 (IL-21) in regulating T-cell activation and communication.

Interleukin-21 is a cytokine that has potent regulatory effects on cells of the immune system, including natural killer (NK) cells and cytotoxic T-cells that can destroy virally infected or cancerous cells. This cytokine induces cell division/proliferation in its target cells. IL-21 elicits its effects on immune cells by interacting with a cell surface receptor known as the interleukin-21 receptor, IL-21R, that is expressed in bone marrow cells and various lymphocytes.

Investigators at the University of Alabama (Birmingham, USA) worked with mice suffering from lymphocytic choriomeningitis, a viral infection of the membranes surrounding the brain and spinal cord. During the study the investigators concentrated on two types of T-cells, CD4 and CD8+ T-cells, before and after the mice were treated with interleukin-21.

Results published in the May 14, 2009, online edition of the journal Science revealed that IL-21 directly influenced the generation of polyfunctional CD8+ T-cells, and that the number of CD4+ T cells that produce IL-21 differed markedly between acute and chronic infections.

"Interleukin-21 served as the key messenger between the T-cells, whereas before we did not know exactly how the two types of cells communicated with each other," said senior author Dr. Allan Zajac, associate professor of microbiology at the University of Alabama. "The CD4 T-cells help the immune system do its job by boosting CD8+ T-cells' ability to fight and kill viruses."

"Adding interleukin-21 back in stimulates the immune response and controls the infection," said Dr. Zajac. "We demonstrate that the loss of this protein prevents the control of the infection and diminishes the function of the killer T-cells, specifically CD8 T-cells."

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