Thus, our data provide a possible explanation for the differential regulation of the immune response in patients with DRB1*07, DRB1*04 and DRB1*11 upon Bb-infection; namely, HLA-DRB1*07, and -DRB1*04 would predispose individuals to chronic disease development by generating an inflammatory milieu for Borrelia, while HLA-DRB1*11 would exert a protective role through the production of anti-spirochetal antibodies, which bind to the bacteria and eliminate it. The gene discussed is HLA-DRB1; the disease is infection.