The immune system is a complex mechanism protecting the body from diseases and illnesses by attacking invading pathogens and viruses. But to work properly, it needs to be able to reach the sights of infection quickly and discern between normal tissues and foreign agents.

In some cases, strong responses by the immune system can cause autoimmune diseases — diseases involving cells which attack the body producing them — such as rheumatoid arthritis and lupus.

This is where regulatory T cells come in to help.

Regulatory T cells

prevent autoimmunity and they do this by suppressing the activation of other immune cells, wrote Jennifer Lund, senior fellow of immunology at the UW, in an e-mail.

However, recent studies by a team at the UW have found that these cells also help in directing quick responses to virus invasions.

The authors of the study, including Lund, Lianne Hsing, an immunology graduate student, Thuy T. Pham, a senior majoring in biology and Alexander Rudensky, a professor of immunology and investigator at the Howard Hughes Medical Institute, have found the results of their study counterintuitive to what was previously predicted.

Regulatory T cells are key in preventing autoimmunity. However, the roles of the cells in immune response to pathogens is not well understood, Rudensky said.

The study involved genetically altered mice deficient in regulatory T cells and how they responded to mucosal viral infections due to a genital herpes virus.

“It was thought that when the body encounters an infection, regulatory T cells would either remain refractory­ — not responding to the presence of the infectious agents — or that they would perform their classic role of suppressing the immune system,” Lund said. “However, we found that in the case of genital herpes simplex-two infection, regulatory T cells are required to coordinate early immune responses that help to protect mice from infection.”

The study found that mice deficient in regulatory T cells were unable to fight off the infections properly. Researchers also found delay in the responses of other types of T cells, dendritic cells and natural killer cells to the site of infection.

“When regulatory T cells were eliminated, the populations of cells that normally respond to HSV-2 infections did not receive the proper cues to migrate to the site of infection, and could therefore not do their job in a timely fashion,” Lund said. “Thus our study points to a novel role for regulatory T cells in the regulation of immune cell-trafficking upon infection.”

The results of the study help shed some light on the role of regulatory T cells in immune response to not just mucosal viral infections like the herpes simplex virus, but also influenza, HIV and other viruses that infect across mucosal surfaces, Lund said.

“It is essential that we have a detailed understanding of how immunity to infection is generated, including which cell types are involved and when, in order to produce the next generation of vaccines and treatments for viral infections,” Lund said.