Borrelia burgdorferi-infected, interleukin-6-deficient mice have decreased Th2 responses and increased lyme arthritis

J. Anguita, M. Rincon, S. Samanta, Stephen W Barthold, R. A. Flavell, E. Fikrig

Research output: Contribution to journalArticle

57 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1512-1515
Number of pages4
JournalJournal of Infectious Diseases
Volume178
Issue number5
DOIs
StatePublished - 1998
Externally publishedYes

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Immunology

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