Host-pathogen interactions in the immunopathogenesis of Lyme disease.
The immunopathogenesis of Lyme disease is complicated and requires a thorough understanding of the interaction among the causative organism, Borrelia burgdorferi, its tick vector, and its mammalian hosts. In vitro, animal and human studies have shown that the organism is capable of adapting to and utilizing elements from its environment to establish infection and persist despite a inducing a strong immune response. Indeed, the immune response may be responsible for many of the symptoms associated with Lyme disease. It appears that humoral immunity plays the greatest role in clearance of the organism. Cytokines released by Th 1 or Th 2 subsets of CD4+ cells have been shown to play an important role in determining outcome of the disease in animal models possibly through their effects on immunoglobulin class switching. In the small percentage of patients who have treatment resistant chronic Lyme disease, autoimmune mechanisms may play a role in persistent disease.
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Tupper Research Institute, Division of Geographic Medicine and Infectious Diseases, New England Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Klempner
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D000818:Animals; D000917:Antibody Formation; D015551:Autoimmunity; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism; D015748:Borrelia burgdorferi Group / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002908:Chronic Disease; D016207:Cytokines / Q000276:immunology; D006790:Host-Parasite Interactions; D006801:Humans; D008193:Lyme Disease / Q000276:immunology*; D051379:Mice; D008806:Mice, Inbred AKR; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D016513:Mice, SCID; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D013987:Ticks / Q000382:microbiology
D016207:Cytokines