Protein in Gonorrhea Bacteria ‘Switches Off’ Immune Response
A protein on the gonorrhea bacterium Neisseria gonorrhoeae "switch[es] off" the immune system's response to the invading organism by binding to receptors on CD4+ T cells, making the body less likely to fight off the infection, according to a study in the advanced online edition of the journal Nature Immunology, Reuters Health reports. Dr. Scott Gray-Owen of the University of Toronto said the protein, Opa52, "squelch[es]" the activation of the CD4+ T cells by binding to a receptor called CEACAM1 and triggering a "chain of events" that prevents the cells from "recognizing the outside invader" and forming antibodies. In contrast, strains of gonorrhea with different types of Opa actually evoke an immune response. The findings "provide hope that a protective vaccine would be effective," Gray-Owen said, adding that part of the Opa52 protein that binds with CEACAM1 receptors would be an "ideal vaccine target." The findings could have an effect on research involving other types of bacteria, such as some that cause meningitis, that also bond to CEACAM1. People infected with gonorrhea are more likely than those without the infection to be co-infected with HIV or chlamydia. Gonorrhea infection lowers the number of CD4+ T cells in individuals with HIV and increases viral levels (McKinney, Reuters Health, 2/20).This is part of the KHN Morning Briefing, a summary of health policy coverage from major news organizations. Sign up for an email subscription.