CD4(+) T helper 1 cells facilitate regression of murine Lyme carditis

Murine Lyme borreliosis, caused by infection with the spirochete Borrelia b urgdorferi, results in acute arthritis and carditis that regress as a resul t of B. burgdorferi-specific immune responses. B. burgdorferi-specific anti bodies can attenuate arthritis in mice deficient in both B cells and T cell s but have no effect on carditis. Because macrophages comprise the principa l immune cell in carditis, T-cell responses that augment cell-mediated immu nity may be important for carditis regression. To investigate this hypothes is, we examined the course of Lyme carditis in mice selectively deficient i n B cells or alpha beta T cells. Our results show that carditis regresses i n B-cell-deficient B10.A(k) mice but not in alpha beta T-cell-deficient mic e, independently of the mouse strain background. Despite prominent macropha ge infiltrates, hearts from B. burgdorferi-infected alpha beta T-cell-defic ient mice had less mRNA for tumor necrosis factor alpha as measured by reve rse transcription-PCR compared to infected control mice. Anti-inflammatory cytokine mRNA levels were equivalent. Adoptive transfer of gamma interferon -secreting CD4(+) T cells into infected alpha beta T-cell-deficient mice pr omoted carditis resolution. These results show that alpha beta T cells can promote resolution of murine Lyme carditis and are the first demonstration of a beneficial role for CD4(+) T helper 1 cells in this disease.