Some of the self-reactive antibodies produced in patients with systemic lupus erythematosus (SLE) were found to neutralize HIV, the virus responsible for causing AIDS, thus protecting patients from the disease.
The findings help explain why SLE patients show lower levels of HIV-1 infection and shed light on ways to promote the production of these antibodies in healthy patients.
A research team in Colorado reported the findings in a study titled, “Breaching peripheral tolerance promotes the production of HIV-1–neutralizing antibodies,” in The Journal of Experimental Medicine.
Some patients infected with HIV-1 make specific antibodies that recognize conserved regions of the HIV-1 virus. These “broadly neutralizing antibodies,” or bnAbs, bind to the surface of the virus — the envelope protein — and protect people from HIV infection.
But because bnAbs often develop many years after HIV infection and in a minority of patients, researchers are working to accelerate their production during HIV vaccination.
The body has a way of preventing the formation of antibodies that attack its own structures. This mechanism, called immunological tolerance, eliminates B-cells producing these antibodies before they have the chance to be harmful. But in patients with autoimmune diseases like SLE, this process is faulty.
Researchers knew that some bnAbs were also self-reactive, which suggested that the production of these antibodies could be halted by the same mechanism that was faulty in SLE. This gave researchers an idea of how to boost the production of bnAbs.
The team wondered if breaching the immunological tolerance would increase antibodies capable of neutralizing HIV-1.
They started testing mice with genetic defects that cause loss of immune tolerance. These mice show lupus-like symptoms because their immune B-cells produce self-reactive antibodies.
The team injected the mice with alum, a chemical that promotes antibody secretion and is often used as an…