Phenotypic analyses of mononuclear cells recovered from healthy and diseased human periodontal tissues

Stoufi, Eleana; Taubman, Martin A.; Ebersole, Jeffrey L.; Smith, Daniel J.; Stashenko, Philip

doi:10.1007/bf00915729

Cited by 93 publications

(86 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…T cell immune reactions to bacteria seem to play a key role in connective tissue destruction and bone resorption in PD (3). T lymphocytes are abundant in diseased periodontal tissue (4). Elevated levels of IgG Ab response to bacterial protein Ags in patients compared with healthy subjects (5) suggests a T cell association with host immune reaction to these bacteria.…”

Section: Requirement Of B7 Costimulation For Th1-mediated Inflammatormentioning

confidence: 99%

“…Both G23 and F13 are CD28 ϩ /␣␤TCR ϩ and proliferate in a MHC class II-and B7-dependent manner. 4 Other characteristics of these T clones, including production of IFN-␥ and IL-2, expression of CD3, CD4, CD25, LFA-1, VLA-4, ICAM-1, and CCR5 by G23, and production of IL-4, expression of CD3, CD4, CD25, LFA-1, VLA-4, and ICAM-1 by F13, have been described previously (21,25). We considered these clones as memory cells based on the following criteria:…”

Section: T Clone Cellsmentioning

confidence: 99%

See 1 more Smart Citation

Requirement of B7 Costimulation for Th1-Mediated Inflammatory Bone Resorption in Experimental Periodontal Disease

Kawai¹,

Eisen-Lev²,

Seki

et al. 2000

The Journal of Immunology

Self Cite

148

192

View full text Add to dashboard Cite

The CD28 costimulation at TCR signaling plays a pivotal role in the regulation of the T cell response. To elucidate the role of T cells in periodontal disease, a system of cell transfer with TCR/CD28-dependent Th1 or Th2 clones was developed in rats. Gingival injection of specific Ag, Actinobacillus actinomycetemcomitans 29-kDa outer membrane protein, and LPS could induce local bone resorption 10 days after the transfer of Ag-specific Th1 clone cells, but not after transfer of Th2 clone cells. Interestingly, the presence of LPS was required not only for the induction of bone resorption but also for Ag-specific IgG2a production. LPS injection elicited the induction of expression of both B7-1 and B7-2 expression on gingival macrophages, which otherwise expressed only MHC class II when animals were injected with Ag alone. The expression of B7 molecules was observed for up to 3 days, which corresponded to the duration of retention of T clone cells in gingival tissues. Either local or systemic administration of CTLA4Ig, a functional antagonist of CD28 binding to B7, could abrogate the bone resorption induced by Th1 clone cells combined with gingival challenge with both Ag and LPS. These results suggest that local Ag-specific activation of Th1-type T cells by B7 costimulation appeared to trigger inflammatory bone resorption, whereas inhibition of B7 expression by CTLA4Ig might be a therapeutic approach for intervention with inflammatory bone resorption.

show abstract

Section: Requirement Of B7 Costimulation For Th1-mediated Inflammatormentioning

confidence: 99%

Section: T Clone Cellsmentioning

confidence: 99%

Requirement of B7 Costimulation for Th1-Mediated Inflammatory Bone Resorption in Experimental Periodontal Disease

Kawai¹,

Eisen-Lev²,

Seki

et al. 2000

The Journal of Immunology

Self Cite

148

192

View full text Add to dashboard Cite

show abstract

“…In terms of the transition from gingivitis to periodontitis, several studies have reported a decreased CD4/CD8 ratio (Taubman et al ., 1984a;Cole et al ., 1987;Stoufi et al ., 1987;Okada et al ., 1988;Wang et al ., 1989) in periodontal lesions, while functional studies have reported a reduced autologous mixed-lymphocyte reaction (Cole et al ., 1987). Taken together, these studies have suggested a local immunoregulatory imbalance.…”

Section: (Iv) Adaptive Immunitymentioning

confidence: 99%

Destructive Periodontitis Lesions are Determined by the Nature of the Lymphocytic Response

Gemmell

Yamazaki²,

Seymour³

2002

Critical Reviews in Oral Biology & Medicine

179

152

View full text Add to dashboard Cite

It is now 35 years since Brandtzaeg and Kraus (1965) published their seminal work entitled "Autoimmunity and periodontal disease". Initially, this work led to the concept that destructive periodontitis was a localized hypersensitivity reaction involving immune complex formation within the tissues. In 1970, Ivanyi and Lehner highlighted a possible role for cell-mediated immunity, which stimulated a flurry of activity centered on the role of lymphokines such as osteoclast-activating factor (OAF), macrophage-activating factor (MAF), macrophage migration inhibition factor (MIF), and myriad others. In the late 1970s and early 1980s, attention focused on the role of polymorphonuclear neutrophils, and it was thought that periodontal destruction occurred as a series of acute exacerbations. As well, at this stage doubt was being cast on the concept that there was a neutrophil chemotactic defect in periodontitis patients. Once it was realized that neutrophils were primarily protective and that severe periodontal destruction occurred in the absence of these cells, attention swung back to the role of lymphocytes and in particular the regulatory role of T-cells. By this time in the early 1990s, while the roles of interleukin (IL)-1, prostaglandin (PG) E2, and metalloproteinases as the destructive mediators in periodontal disease were largely understood, the control and regulation of these cytokines remained controversial. With the widespread acceptance of the Th1/Th2 paradigm, the regulatory role of T-cells became the main focus of attention. Two apparently conflicting theories have emerged. One is based on direct observations of human lesions, while the other is based on animal model experiments and the inability to demonstrate IL-4 mRNA in gingival extracts. As part of the "Controversy" series, this review is intended to stimulate debate and hence may appear in some places provocative. In this context, this review will present the case that destructive periodontitis is due to the nature of the lymphocytic infiltrate and is not due to periodic acute exacerbations, nor is it due to the so-called virulence factors of putative periodontal pathogens.

show abstract

“…A protective role for T cell subsets against periodontal tissue destruction has been suggested in a rat model [4], and involvement of a T cell regulatory imbalance in human chronic periodontal disease has also been demonstrated [5,6].…”

Section: Introductionmentioning

confidence: 99%

Selective expansion of T cells in gingival lesions of patients with chronic inflammatory periodontal disease

Yamazaki

Nakajima

Ohsawa

et al. 2000

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYChronic inflammatory periodontal diseases are characterized by a cellular infiltrate and are similar in many respects to other chronic inflammatory diseases. While periodontopathic bacteria have been recognized as the principal causative agent and the immune response to these bacteria is thought to be responsible for the tissue destruction, the full aetiological spectrum is still incompletely understood. In addition to many cell types such as polymorphonuclear leucocytes and macrophages, T cells have been implicated in pathogenesis and are considered to have regulatory roles in progression of the disease. Based on our recent studies demonstrating biased expression of several Vb families in periodontitis tissues, the aim of this study was to characterize further the T cells relevant to the disease process by reverse transcription-polymerase chain reaction-single-strand conformation polymorphism (RT-PCR-SSCP) and subsequent nucleotide sequence analysis of complementarity-determining region 3 (CDR3) of the TCR b-chain. In spite of the likely involvement of numerous bacteria, the present study has clearly shown the oligoclonality of infiltrating T cells in periodontitis lesions in contrast to low clonality of peripheral blood T cells as evidenced by the appearance of distinct bands in gingival tissue samples and smear pattern of peripheral blood on SSCP gels. These were confirmed by the DNA sequencing of the CDR3 of Vb 16 of selected samples. The analysis of deduced amino acid sequences demonstrated amino acid motifs in the CDR3 region of the periodontitis lesion-derived sequences from each patient. The results indicate that gingival tissue-infiltrating T cells recognizing a limited number of antigens or epitopes are involved in the disease process.

show abstract

Phenotypic analyses of mononuclear cells recovered from healthy and diseased human periodontal tissues

Cited by 93 publications

References 34 publications

Requirement of B7 Costimulation for Th1-Mediated Inflammatory Bone Resorption in Experimental Periodontal Disease

Requirement of B7 Costimulation for Th1-Mediated Inflammatory Bone Resorption in Experimental Periodontal Disease

Destructive Periodontitis Lesions are Determined by the Nature of the Lymphocytic Response

Selective expansion of T cells in gingival lesions of patients with chronic inflammatory periodontal disease

Contact Info

Product

Resources

About