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Infection and Immunity, June 1999, p. 2804-2809, Vol. 67, No. 6
Biology Department, Bates College, Lewiston,
Maine 042401; Department of Oral
Biology, State University of New York, Buffalo, New York
142142; School of Dental Hygiene,
University of New England, Portland, Maine
040923; and The Jackson Laboratory, Bar
Harbor, Maine 046094
Received 11 January 1999/Accepted 9 March 1999
In this study, we used a mouse model to examine the role of the
adaptive immune response in alveolar bone loss induced by oral
infection with the human gram-negative anaerobic bacterium Porphyromonas gingivalis. Severe combined immunodeficient
mice, which lack B and T lymphocytes, exhibited considerably less bone loss than did immunocompetent mice after oral infection, suggesting that lymphocytes contribute to this process. Bone loss after oral infection was decreased in mice deficient in major histocompatibility complex (MHC) class II-responsive CD4+ T cells, but no
change in bone loss was observed in mice deficient in MHC class
I-responsive CD8+ T cells or NK1+ T cells. Mice
lacking the cytokine gamma interferon or interleukin-6 also
demonstrated decreased bone loss. These results suggest that the
adaptive immune response, and in particular CD4+ T cells
and the proinflammatory cytokines that they secrete, are important
effectors of bone loss consequent to P. gingivalis oral
infection. The studies also reinforce the utility of the mouse oral
infection model in dissecting the pathobiology of periodontal disease.
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
CD4+ T Cells and the Proinflammatory Cytokines Gamma
Interferon and Interleukin-6 Contribute to Alveolar Bone Loss in
Mice
*
Corresponding author. Mailing address: Biology
Department, Bates College, Lewiston, ME 04240. Phone: (207) 786 6108. Fax: (207) 786 8334. E-mail: pbaker{at}abacus.bates.edu.
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