Virus infection can trigger the onset of autoimmune diseases, such as acute disseminated encephalomyelitis. For this disease, after the virus is infected, the body begins to attack a protein that protects the nerves of the brain and spinal cord. However, how the virus infects the immune system interacts to trigger an autoimmune response is still a mystery.
Researchers at the University of Basel in Switzerland and the Whitehead Institute in the United States have reported that when B cells interact directly with virus-infected cells, they trigger an unexpected chain reaction. The study was published in the Journal of the American Academy of Sciences (PNAS).
"It's as if you have pulled out your wallet from the bag and pulled out your scarf." The accidental capture of the virus antigens could pass through with the other ones, "said Nicholas Sanderson, the first author of the article at the University of Basel in Switzerland. Immune cell interactions that elicit an autoimmune response.
To explore this phenomenon, the researchers developed cells expressing myelin oligodendrocyte glycoprotein (MOG, with GFP) and influenza hemagglutinin (HA), and then introduced transgenic B cells that specifically recognize MOG or HA The MOG is an antigens, and HA is a viral antigen.
They found that GOG-labeled MOGs were able to capture GFP-labeled transgenic B cells, regardless of the presence or absence of HA. However, when HA is present, GM-identified transgenic B cells also capture GFP-labeled MOGs. Therefore, B cells that specifically capture HA can also capture their own antigen MOG.
"Once B cells are exposed to cells expressing HA and GFP-fusion proteins, they begin to swallow it, and within a few minutes B cells are filled with the protein, which has bite the membrane of the transfected cells, Sanderson said.
This accidental cohort of HA is not due to B cell phagocytosis of each protein in the pathway. Further experiments show that not all proteins expressed on the membrane are co-captured. This phenomenon may be due to the same location on the membrane, or some other direct interaction. The viral antigens expressed on the membrane make them appear to be more likely to be captured by B cells.
Other experiments have also confirmed that antiviral T cells recognize B cells to absorb viral antigens that trigger a response to the virus. However, if B cells also capture other antigens, T cells also recognize autoantigens MOG. This accidental phenomenon caused the production of autoantibodies, the final attack on the MOG, leading to the occurrence of acute disseminated encephalomyelitis.
Sanderson said: "This process is so active, so fast, leading to a large number of B cell activation, let us feel that this can not be experimental illusion. This must happen with some physiological phenomena related to." Researchers are now aware of the virus infected human Whether the process occurred in the organization.