ArticleImmunology1998
Antigen direction of specific T-cell clones into gingival tissues.
Article in Immunology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 52 citations in OpenAlex.
- Toll-Like Receptor Signaling and Immune Regulatory Lymphocytes in Periodontal Disease.International journal of molecular sciences · 2020Review
- Phenotype and Function of Myeloid-Derived Suppressor Cells Induced by Porphyromonas gingivalis Infection.Infection and immunity · 2017Article
- RANKL expression in periodontal disease: where does RANKL come from?BioMed research international · 2014Review
- Perturbation of the indigenous rat oral microbiome by ciprofloxacin dosing.Molecular oral microbiology · 2013Article
- Porphyromonas gingivalis infection-associated periodontal bone resorption is dependent on receptor activator of NF-κB ligand.Infection and immunity · 2013Article
- Role of TLR2-dependent IL-10 production in the inhibition of the initial IFN-γ T cell response to Porphyromonas gingivalis.Journal of leukocyte biology · 2013Article
- Genetic or pharmaceutical blockade of phosphoinositide 3-kinase p110δ prevents chronic rejection of heart allografts.PloS one · 2012Article
- Antibody to receptor activator of NF-κB ligand ameliorates T cell-mediated periodontal bone resorption.Infection and immunity · 2011Article
- Role of periodontal pathogenic bacteria in RANKL-mediated bone destruction in periodontal disease.Journal of oral microbiology · 2010Article
- Memory T-cell trafficking: new directions for busy commuters.Immunology · 2010Review
- Expression of receptor activator of nuclear factor-kappaB ligand by B cells in response to oral bacteria.Oral microbiology and immunology · 2009Article
- T cell receptor-induced phosphoinositide-3-kinase p110delta activity is required for T cell localization to antigenic tissue in mice.The Journal of clinical investigation · 2008Article
- Expression of major histocompatibility complex class II and CD80 by gingival epithelial cells induces activation of CD4+ T cells in response to bacterial challenge.Infection and immunity · 2005Article
- Expression of mucosal homing receptor alpha4beta7 is associated with enhanced migration to the Chlamydia-infected murine genital mucosa in vivo.Infection and immunity · 2000Article
- A novel factor isolated from Actinobacillus actinomycetemcomitans stimulates mouse B cells and human peripheral blood mononuclear cells.Infection and immunity · 2000Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
This study was performed to investigate T-cell traffic to periodontal tissues during infection with a periodontal pathogen Actinobacillus actinomycetemcomitans (Aa). Rowett rat T-cell clones, A3 (CD4+ CD8-, alpha beta TCR+, NKRP-1-, specific to Aa) and G2 (CD4- CD8-, alpha beta TCR+, NKRP-1+, which reacts to Aa, Gram-negative and -positive bacteria), both expressed the same prominent adhesion molecules (LFA-1, VLA-4) to the same extent. Binding of both T-cell clones to rat endothelial cells in vitro was blocked by antibody to VLA-4. Rowett rats were infected with Aa and infused with Aa-stimulated, isogenic T-clone lymphocytes that had been labelled in vitro with 125IUdR. Radioactivity associated with recovery of clone A3, but not G2, was significantly elevated in the gingivae of infected rats, suggesting migration to infected animals' gingival tissues. Migration of radioactive Aa-specific A3 clone cells traced by autoradiography reached a maximum at 24 hr (1.2% of total lymphocytes as radiolabelled cells in infected gingiva versus 0.6% in noninfected), indicating an apparent antigen-directed retention in infected rats' gingival tissues. The G2 clone was not retained in the gingival tissues (0.20% of total lymphocytes as radiolabelled cells in infected gingiva versus 0.26% in non-infected). However, the possibility of A3 retention directed by inflammation or tissue-selective homing could not be excluded. In further experiments, other adoptively transferred T-clone lymphocytes [clones G23 (Th1) and F13 (Th2)] with specificity for the 29,000 MW outer membrane protein of Aa with the same prominent adhesion molecules could be recovered from rat gingivae previously challenged with this antigen. However, transferred T-clone lymphocytes [clone G26 (Th1)] with specificity for a different Aa antigen were not recovered. Therefore, the dynamics of cell entry into periodontal lesions vary for activated T lymphocytes with different antigenic specificities, indicating the significance of antigen in lymphocyte traffic to periodontal tissues.
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