Journal
JOURNAL OF IMMUNOLOGY
Volume 200, Issue 4, Pages 1457-1470Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1701248
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Funding
- National Institutes of Allergy and Infectious Disease [T32 AI055434]
- American Association of Immunologists Careers in Immunology Fellowship Program
- Edward Mallinckrodt Jr. Foundation
- Pew Charitable Trusts Scholars Program
- National Science Foundation CAREER Award [IOS-1253278]
- David and Lucile Packard Foundation Fellowship in Science and Engineering
- National Institute of Allergy and Infectious Diseases [K22 AI95375, AI107090, AI109122]
- National Institutes of Health [DP2AT008746, R01 AI32223, R01 AR43521, R21AI114462]
- National Center for Research Resources/National Institutes of Health [1S10RR026802-01]
- NATIONAL CENTER FOR COMPLEMENTARY & ALTERNATIVE MEDICINE [DP2AT008746] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [S10RR026802] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [N01AI095375, K22AI095375, R21AI114462, T32AI055434, R01AI032223, R21AI109122, R56AI107090] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR043521] Funding Source: NIH RePORTER
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T cells predominate the immune responses in the synovial fluid of patients with persistent Lyme arthritis; however, their role in Lyme disease remains poorly defined. Using a murine model of persistent Lyme arthritis, we observed that bystander activation of CD4(+) and CD8(+) T cells leads to arthritis-promoting IFN-gamma, similar to the inflammatory environment seen in the synovial tissue of patients with posttreatment Lyme disease. TCR transgenic mice containing monoclonal specificity toward non-Borrelia epitopes confirmed that bystander T cell activation was responsible for disease development. The microbial pattern recognition receptor TLR2 was upregulated on T cells following infection, implicating it as marker of bystander T cell activation. In fact, T cellintrinsic expression of TLR2 contributed to IFN-gamma production and arthritis, providing a mechanism for microbial-induced bystander T cell activation during infection. The IL-10-deficient mouse reveals a novel TLR2-intrinsic role for T cells in Lyme arthritis, with potentially broad application to immune pathogenesis.
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