title: Borrelia burgdorferi Pathogenesis and the Immune Response.
abstract: Borrelia burgdorferi is the tick-borne etiologic agent of Lyme disease. The spirochete must negotiate numerous barriers in order to establish a disseminated infection in a mammalian host. These barriers include migration from the feeding tick midgut to the salivary glands, deposition in skin, manipulation or evasion of the localized host immune response, adhesion to and extravasation through an endothelial barrier, hematogenous dissemination, and establishment of infection in distal tissue sites. Borrelia burgdorferi proteins that mediate many of these processes and the nature of the host response to infection are described.
authors.affiliation: Department of Microbiology and Immunology, New York Medical College, Valhalla, NY 10595, USA.
authors.forename: Mary
authors.initials: M
authors.lastname: Petzke
authors.affiliation: Department of Microbiology and Immunology, New York Medical College, Valhalla, NY 10595, USA. Electronic address: schwartz@nymc.edu.
authors.forename: Ira
authors.initials: I
authors.lastname: Schwartz
mesh_terms: D000818:Animals; D000942:Antigens, Bacterial / Q000032:analysis; D025065:Borrelia burgdorferi / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity*; D006801:Humans; D057131:Immune Evasion; D007113:Immunity, Innate; D016023:Integrins / Q000378:metabolism
chemical_list: D000942:Antigens, Bacterial; D016023:Integrins
keywords: Adhesins; Genotypic variation; Immune evasion; Lyme disease; Type I interferon