| First Author | Whiteside SK | Year | 2018 |
| Journal | J Immunol | Volume | 200 |
| Issue | 4 | Pages | 1457-1470 |
| PubMed ID | 29330323 | Mgi Jnum | J:257126 |
| Mgi Id | MGI:6116063 | Doi | 10.4049/jimmunol.1701248 |
| Citation | Whiteside SK, et al. (2018) IL-10 Deficiency Reveals a Role for TLR2-Dependent Bystander Activation of T Cells in Lyme Arthritis. J Immunol 200(4):1457-1470 |
| abstractText | 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 cell-intrinsic 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. |
