Recently, three different papers in Science Immunology have demonstrated that it is type I interferon (IFN-I) that inhibits the production of neutralizing antibodies in chronic infections such as LCMV infection.
LCMV, which is an abbreviation for lymphocytic choriomeningitis virus, is a pathogen, normally carried in rodents, which can cause aseptic meningitis and other diseases in humans. This virus is a well model to study T-cell immune responses. The reason is that antibody production by B cells is often weakened during LCMV infection. Some other viruses such as HBV and HIV also don’t trigger strong antibody responses. Why antibody production is suppressed during these viral infections remains a mystery. Now, the three new studies have revealed that IFN-I is the cause of this suppression.
In one of the studies, Dorian McGavern and colleagues from the National Institute of Neurological Disorders and Stroke modified B cells to recognize LCMV. If mice received the B cells before exposure to LCMV, these cells disappeared from the spleen quickly. In contrast, if mice received the B cells after exposure to LCMV, these cells stuck around. The study also showed that much IFN-I was produced over the first few days of LCMV infection.
IFN-I is a subgroup of cytokines that functions to regulate immune responses. It is known to provide protection against viral infections. But during LCMV infection, IFN-I appears to have harmful effect.
McGavern’s team also found that inhibition of the IFN-I receptor before infection resulted in a great increase in the number of LCMV-specific B cells in infected mice’s spleen. These cells generated many antibodies against the virus.
Furthermore, McGavern’s team discovered that in response to IFN-I, CD8+ T cells could contact with and destroy B cells. In another study, Daniel Pinschewer from the University of Basel also found that T cells, dendritic cells and myeloid cells together contributed to B-cell loss in response to IFN-I. CusAb-Flarebio offers IFN-I and rabbit polyclonal antibody against it.
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