Inhibitory Signals Mediated by Programmed Death‐1 Are Involved With T‐Cell Function in Chronic Periodontitis

Figueira, Eduardo Aleixo; Rezende, Maria Lúcia Rubo de; Torres, Sérgio Aparecido; Garlet, Gustavo; Lara, Vanessa Soares; Santos, Carlos; Avila-Campos, Mario Júlio; Silva, João; Campanelli, Ana Paula

doi:10.1902/jop.2009.090057

Cited by 22 publications

(13 citation statements)

References 46 publications

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“…The role of CD8 + T‐cells in periodontitis has been analyzed in patients with different forms of periodontitis . CD8 + T‐cell clones from inflamed periodontal tissues were analyzed in early studies, by stimulation with phytohemagglutinin, for their production of different cytokines and their biological functions.…”

Section: Role Of Cytotoxic T‐cell Subsets In Periodontitismentioning

confidence: 99%

T‐ and B‐cell subsets in periodontitis

Gonzáles¹

2015

Periodontology 2000

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A large amount of information is available, in the medical literature, on the molecular and immunological mechanisms in which T- and B-cells are involved in the pathogenesis of inflammatory diseases. This review attempts to describe the most important features of the T-cell subsets and their cytokine networks in periodontitis, including the interaction of pathogens with different cell subsets and their gene-expression profiles. Additionally, the known interactions of T- and B-cell subsets in periodontitis are described. The purpose of this article was to provide an overview of the cell interactions and cytokine networks specifically involved in the pathogenesis of periodontitis, and models and paradigms from recent research in this area are presented. However, the review of the literature also revealed that relatively little is known about the genetic or structural factors that confer cross-reactivity of natural and/or autoreactive antibodies in the immunopathogenesis of periodontitis. Pathogens, in turn, are continuously evolving and creating mechanisms to evade immunological reactions controlled and modulated by T- and B-cells.

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Section: Role Of Cytotoxic T‐cell Subsets In Periodontitismentioning

confidence: 99%

T‐ and B‐cell subsets in periodontitis

Gonzáles¹

2015

Periodontology 2000

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“…Earlier studies (do Vale et al, 2004;Figueira et al, 2009) showed that peripheral blood mononuclear cells from patients with periodontitis did not proliferate in response to bacterial antigens. However, other studies (Pejcic et al, 2011;Gaddale et al, 2014) have confirmed an increased number of WBCs and neutrophils in the peripheral blood of patients with moderate to severe periodontitis, with a positive correlation between disease severity and number of WBCs in the blood.…”

Section: Discussionmentioning

confidence: 99%

Role of Cytokines and Transcription Factors in Periodontitis: A Review of Cellular and Molecular Mechanisms

Leite¹,

Carneiro²,

Nunes

et al. 2015

American Journal of Immunology

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Periodontal Diseases (PD) are characterized by pathological manifestation of host immune response to bacterial infection at the tooth/gingival interface. Evidences points periodontitis as a risk factor for pathological systemic conditions, such as, cardiovascular diseases and diabetes. The identification of host factors that determine their susceptibility to immune subversion can provide useful information in the pathogenesis of periodontitis. Protective acute inflammatory response fails to remove inflammatory cells, especially neutrophils, evolving to chronic, destructive and pathological lesions. T and B cells actively participate in pathogenesis of the disease. CD4+ naive T cells are activated by antigenic stimulation and differentiate into subpopulations of distinct effector cells, characterized by its specific cytokine production profiles and functions. In periodontal infection, activated Th17 and regulatory T lymphocytes (Tregs) play antagonistic roles as effector and suppressor cells, respectively. In presence of Tregs, there is a decrease in the levels of pro-inflammatory cytokines, such as, Interferon gamma (IFN-γ), Interleukin (IL) -17, Tumor Necrosis Factor (TNF) and IL-1 β, at sites of disease. Absence of Tregs may cause a variety of disorders, such as, periodontitis. The RANKL/RANK system and Osteoprotegerin (OPG) are modulators of bone resorption in periodontitis. The balance between periodontal bone resorption by osteoclasts and bone formation by osteoblasts controls bone mass. RANKL induces osteoclast differentiation and maturation and OPG inhibits RANK/RANKL interaction and prevents bone resorption. RANKL mRNA and the RANKL/OPG mRNA ratio were enhanced in chronic periodontitis. Furthermore, the role of NF-kB, FoxP3 and T-bet transcription factors were explored. Therapies for periodontitis involving cellular and molecular biology are not specific and have many side effects. Current therapies to successfully control the PD reduces clinical signs of inflammation at local sites of the disease; however, new treatments for periodontitis should address the contribution of immune cells in bone resorption, particularly in the natural course of the disease, considering its periods of remission and progression.

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“…In gingival tissue from chronic periodontitis, a marked increase in total CD4 + T cells, CD8 + T cells, and B cells, akin to neutrophils, was observed, and most of the CD4 + T cells produced IL-17 ( 34 ). Although in the study of Dutzan et al CD8 + Treg are not detected in the gingiva of chronic periodontitis patients ( 34 ), previous studies showed that some gingival CD8 + T cells lack CD28 while expressing the inhibitory receptor PD1 ( 35 – 37 ). These features are associated with an effector–memory phenotype ( 20 ).…”

Section: Gingival Cd8 + T Cells and Chronic Periodmentioning

confidence: 93%

“…Given the effector–memory phenotype ( 34 – 37 ), and unlike CD4 + T cells that express CD28 and may respond to TCR/CD28-mediated signals, gingival CD8 + T cells may preferentially be activated in a TCR-independent manner by local signals produced during stress and/or injury, including a variety of endogenous products that signal through innate receptors, as discussed elsewhere ( 20 ). As a result, upon innate receptor triggering gingival CD8 + T cells may secrete cytokines, such as IL-10 and IFN-γ, reported to have bone repairing properties ( 23 , 26 ).…”

Section: Gingival Cd8 + T Cells: Molecular Signalsmentioning

confidence: 99%