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Infection and Immunity, September 2001, p. 5264-5269, Vol. 69, No. 9
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.9.5264-5269.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

CD4+ T Helper 1 Cells Facilitate Regression of Murine Lyme Carditis

Linda K. Bockenstedt,1,* Insoo Kang,1 Christopher Chang,1,dagger David Persing,2,Dagger Adrian Hayday,3,4,§ and Stephen W. Barthold5

Department of Internal Medicine,1 and Section of Immunobiology,3 Yale University School of Medicine, and Department of Biology, Yale University,4 New Haven, Connecticut 06520; Department of Laboratory Medicine, Mayo Clinic, Rochester, Minnesota 559052; and Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California, Davis, California 956165

Received 12 February 2001/Returned for modification 10 April 2001/Accepted 21 May 2001

Murine Lyme borreliosis, caused by infection with the spirochete Borrelia burgdorferi, results in acute arthritis and carditis that regress as a result of B. burgdorferi-specific immune responses. B. burgdorferi-specific antibodies can attenuate arthritis in mice deficient in both B cells and T cells but have no effect on carditis. Because macrophages comprise the principal immune cell in carditis, T-cell responses that augment cell-mediated immunity may be important for carditis regression. To investigate this hypothesis, we examined the course of Lyme carditis in mice selectively deficient in B cells or alpha beta T cells. Our results show that carditis regresses in B-cell-deficient B10.Ak mice but not in alpha beta T-cell-deficient mice, independently of the mouse strain background. Despite prominent macrophage infiltrates, hearts from B. burgdorferi-infected alpha beta T-cell-deficient mice had less mRNA for tumor necrosis factor alpha as measured by reverse 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 promoted 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.

* Corresponding author. Mailing address: Section of Rheumatology, Yale University School of Medicine, 333 Cedar St., P.O. Box 208031, New Haven, CT 06520-8031. Phone: (203) 785-7063. Fax: (203) 785-7053. E-mail: linda.bockenstedt{at}yale.edu.

dagger Present address: Department of Surgery, Duke University Medical Center, Durham, NC 27705.

Dagger Present address: Diagnostics Research, Corixa Corp., Seattle, WA 98104.

§ Present address: Department of Immunobiology, Medical Schools of Guy's, King's, and St. Thomas's, University of London, London SE1 9RT, United Kingdom.

Infection and Immunity, September 2001, p. 5264-5269, Vol. 69, No. 9
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.9.5264-5269.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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