Many viruses, such as West Nile, Zika, and the herpes simplex virus enter the nervous system, where they were thought to be beyond the reach of antibodies. Researchers used mice models to investigate how antibodies could gain access to nerve tissue in order to control infection.

In mice infected with herpes, they observed a previously under-recognized role of CD4 T cells, a type of white blood cell that guards against infection by sending signals to activate immunity. In response to herpes infection, CD4 T cells entered the nerve tissue, secreted signaling proteins, and allowed antibody access to infected sites. Combined, CD4 T cells and antibodies limited viral spread.

Authors show that memory CD4 T cells migrate to the dorsal root ganglia and spinal cord in response to infection with herpes simplex virus type 2. Once inside these neuronal tissues, CD4 T cells secrete interferon-γ and mediate local increase in vascular permeability, enabling antibody access for viral control.

A similar requirement for CD4 T cells for antibody access to the brain is observed after intranasal challenge with vesicular stomatitis virus. 

"This is a very elegant design of the immune system to allow antibodies to go to the sites of infection," said the senior author. "The CD4 T cells will only go to the site where there is a virus. It's a targeted delivery system for antibodies."

The implications of the finding are multiple. Without CD4 T cells, antibody-based therapies that are being developed for conditions like herpes may not be sufficient to control infection, author noted. Conversely, for antibody-mediated autoimmune diseases such as Guillain-Barre, "it may be beneficial to block CD4 from entering the neuronal tissues," she said.

http://news.yale.edu/2016/05/18/yale-study-how-antibodies-access-neurons-fight-infection