Lymphocyte subpopulation in healthy and diseased gingival tissue

Amunulla, Aniz; Venkatesan, Remya; Hemalatha, R.; Arun, KV; Sudarshan, Sabitha; Talwar, Avaneendra

doi:10.4103/0972-124x.44091

Cited by 7 publications

(1 citation statement)

References 22 publications

(30 reference statements)

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“…It is known that Th cell responses provide the necessary cytokines for proliferation of B cells and their polyclonal activation, facilitated by the presence of LPS, leading to high levels of antibodies and continuous production of IL-1β, which contributes to bone resorption (Amunulla et al, 2008;Gaffen and Hajishengallis, 2008).…”

Section: The Microbial Challenge: Cellular and Molecular Mechanisms Imentioning

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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Section: The Microbial Challenge: Cellular and Molecular Mechanisms Imentioning

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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Porphyromonas gingivalis antigens differently participate in the proliferation and cell death of human PBMC

Trindade¹,

Olczak²,

Filho³

et al. 2012

Archives of Oral Biology

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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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Lymphocyte subpopulation in healthy and diseased gingival tissue

Cited by 7 publications

References 22 publications

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

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

Porphyromonas gingivalis antigens differently participate in the proliferation and cell death of human PBMC

T‐ and B‐cell subsets in periodontitis

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