title: T-cell contributions to alveolar bone loss in response to oral infection with Porphyromonas gingivalis.
abstract: We have previously shown that mice lacking CD4+, but not CD8+, T cells lose less alveolar bone loss in response to oral infection with Porphyromonas gingivalis than do immunocompetent mice of the same genetic background, indicating that CD4+ T cells contribute to bone resorption. The CD4+ and CD8+ T-cell knockouts were produced by targeted deletions of, respectively, major histocompatibility complex II (MHCII) or beta2-microglobulin (producing non-expression of MHCI). Because MHC deletions can have other effects in addition to those on T-cell selection, we wanted to confirm that the lessened bone loss was truly an effect of the lack of T cells. Consequently, we repeated our experiments with C57B1 /6J-Tcra mice that have a targeted deletion of the alpha chain of the T-cell receptor (Tcra). Six weeks after oral infection with P. gingivalis ATCC 53977 the total bone loss at buccal maxillary sites was 0.28 mm in infected immunocompetent mice (P=0.002 compared with sham-infected mice), whereas in Tcra knockouts the bone loss was only 0.08 mm (P=0.04 compared with shams). The T-cell-deficient mice thus lost 70% less bone after infection than did genetically matched immunocompetent mice (P =0.003). These experiments confirm that T cells, and their responses to oral infection with P. gingivalis, help to push bone remodeling in the direction of net loss of bone.
authors.affiliation: Biology Department, Bates College, Lewiston, Maine 04210, USA. pbaker@bates.edu
authors.forename: P J
authors.initials: PJ
authors.lastname: Baker
authors.forename: J
authors.initials: J
authors.lastname: Garneau
authors.forename: L
authors.initials: L
authors.lastname: Howe
authors.forename: D C
authors.initials: DC
authors.lastname: Roopenian
mesh_terms: D016301:Alveolar Bone Loss / Q000276:immunology* / Q000382:microbiology*; D000818:Animals; D016866:Bacteroidaceae Infections / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D002352:Carrier Proteins / Q000096:biosynthesis / Q000276:immunology; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D007371:Interferon-gamma / Q000276:immunology; D015850:Interleukin-6 / Q000096:biosynthesis / Q000276:immunology; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016966:Porphyromonas gingivalis / Q000472:pathogenicity*; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000276:immunology
chemical_list: D002352:Carrier Proteins; D000949:Histocompatibility Antigens Class II; D015850:Interleukin-6; D008562:Membrane Glycoproteins; D053245:RANK Ligand; D053246:Receptor Activator of Nuclear Factor-kappa B; D016693:Receptors, Antigen, T-Cell, alpha-beta; C505687:Tnfrsf11a protein, mouse; C505689:Tnfsf11 protein, mouse; D007371:Interferon-gamma