| First Author | Anguita J | Year | 1998 |
| Journal | J Infect Dis | Volume | 178 |
| Issue | 5 | Pages | 1512-5 |
| PubMed ID | 9780277 | Mgi Jnum | J:51191 |
| Mgi Id | MGI:1314816 | Doi | 10.1086/314448 |
| Citation | Anguita J, et al. (1998) Borrelia burgdorferi-infected, interleukin-6-deficient mice have decreased Th2 responses and increased lyme arthritis. J Infect Dis 178(5):1512-5 |
| abstractText | Recently, interleukin (IL)-6 was shown to be one of the earliest factors that trigger the differentiation of naive T cells into effector Th2 cells in vitro. Lyme arthritis was studied in IL-6-deficient mice, since joint inflammation is influenced by the T helper cell response against Borrelia burgdorferi. Arthritis incidence increased in B. burgdorferi-infected IL-6-deficient mice compared with that in controls. Furthermore, splenocytes of B. burgdorferi-infected IL-6-deficient mice produced significantly less IL-4 in response to Borrelia antigens than did C57BL/6 (B6) mice, and B. burgdorferi-specific IgG2b levels were significantly reduced in IL-6-deficient mice at 60 days of infection. These results extend previous in vitro observations by demonstrating an in vivo role for IL-6 in the differentiation of CD4 T cells toward a Th2 phenotype and further show that CD4 T cell responses influence murine Lyme arthritis. |
