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*
Department of Pathology, University of Utah, Salt Lake City, UT 84132;
Department of Veterinary Pathobiology, University of Illinois, Urbana, IL 61801; and
Institute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich, Munich, Germany
Borrelia burgdorferi lipoproteins activate inflammatory cells through Toll-like receptor 2 (TLR2), suggesting that TLR2 could play a pivotal role in the host response to B. burgdorferi. TLR2 does play a critical role in host defense, as infected TLR2-/- mice harbored up to 100-fold more spirochetes in tissues than did TLR2+/+ littermates. Spirochetes persisted at extremely elevated levels in TLR2-deficient mice for at least 8 wk following infection. Infected TLR2-/- mice developed normal Borrelia-specific Ab responses, as measured by quantity of Borrelia-specific Ig isotypes, the kinetics of class switching to IgG, and the complexity of the Ags recognized. These findings indicate that the failure to control spirochete levels in tissues is not due to an impaired acquired immune response. While macrophages from TLR2-/- mice were not responsive to lipoproteins, they did respond to nonlipoprotein components of sonicated spirochetes. These TLR2-independent responses could play a role during the inflammatory response to B. burgdorferi, as infected TLR2-/- mice developed greater ankle swelling than wild-type littermates. Thus, while TLR2-dependent signaling pathways play a major role in the innate host defense to B. burgdorferi, both inflammatory responses and the development of the acquired humoral response can occur in the absence of TLR2.
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I. Diterich, C. Rauter, C. J. Kirschning, and T. Hartung Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via Immunosuppression Infect. Immun., July 1, 2003; 71(7): 3979 - 3987. [Abstract] [Full Text] [PDF]
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R. B. Oliveira, M. T. Ochoa, P. A. Sieling, T. H. Rea, A. Rambukkana, E. N. Sarno, and R. L. Modlin Expression of Toll-Like Receptor 2 on Human Schwann Cells: a Mechanism of Nerve Damage in Leprosy Infect. Immun., March 1, 2003; 71(3): 1427 - 1433. [Abstract] [Full Text] [PDF]
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U. Koedel, B. Angele, T. Rupprecht, H. Wagner, A. Roggenkamp, H.-W. Pfister, and C. J. Kirschning Toll-Like Receptor 2 Participates in Mediation of Immune Response in Experimental Pneumococcal Meningitis J. Immunol., January 1, 2003; 170(1): 438 - 444. [Abstract] [Full Text] [PDF]
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A. Sing, D. Rost, N. Tvardovskaia, A. Roggenkamp, A. Wiedemann, C. J. Kirschning, M. Aepfelbacher, and J. Heesemann Yersinia V-Antigen Exploits Toll-like Receptor 2 and CD14 for Interleukin 10-mediated Immunosuppression J. Exp. Med., October 21, 2002; 196(8): 1017 - 1024. [Abstract] [Full Text] [PDF]
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B. T. Edelson and E. R. Unanue MyD88-Dependent but Toll-Like Receptor 2-Independent Innate Immunity to Listeria: No Role for Either in Macrophage Listericidal Activity J. Immunol., October 1, 2002; 169(7): 3869 - 3875. [Abstract] [Full Text] [PDF]
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H. Weighardt, S. Kaiser-Moore, R. M. Vabulas, C. J. Kirschning, H. Wagner, and B. Holzmann Cutting Edge: Myeloid Differentiation Factor 88 Deficiency Improves Resistance Against Sepsis Caused by Polymicrobial Infection J. Immunol., September 15, 2002; 169(6): 2823 - 2827. [Abstract] [Full Text] [PDF]
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J. Anguita, S. W. Barthold, R. Persinski, M. N. Hedrick, C. A. Huy, R. J. Davis, R. A. Flavell, and E. Fikrig Murine Lyme Arthritis Development Mediated by p38 Mitogen-Activated Protein Kinase Activity J. Immunol., June 15, 2002; 168(12): 6352 - 6357. [Abstract] [Full Text] [PDF]
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