Borrelia burgdorferi-infected, interleukin-6-deficient mice have decreased Th2 responses and increased lyme arthritis.
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.
Section of Rheumatology, Department of Internal Medicine, Howard Hughes Medical Institute, New Haven, Connecticut, USA.
J
J
Anguita
M
M
Rincón
S
S
Samanta
S W
SW
Barthold
R A
RA
Flavell
E
E
Fikrig
D000818:Animals; D000907:Antibodies, Bacterial / Q000096:biosynthesis; D015748:Borrelia burgdorferi Group / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000502:physiology; D016764:Cell Polarity; D015850:Interleukin-6 / Q000172:deficiency* / Q000502:physiology; D008193:Lyme Disease / Q000276:immunology* / Q000382:microbiology; D051379:Mice; D008810:Mice, Inbred C57BL; D009205:Myocarditis / Q000276:immunology / Q000382:microbiology; D018418:Th2 Cells / Q000276:immunology*
D000907:Antibodies, Bacterial; D015850:Interleukin-6