T cells, teeth and tissue destruction – what do T cells do in periodontal disease?

Campbell, Louisa; Millhouse, Emma; Malcolm, Jennifer; Culshaw, Shauna

doi:10.1111/omi.12144

Cited by 49 publications

(58 citation statements)

References 88 publications

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“…The subpopulation of lymphocytes T-helper CD4+ that will predominate against a stimulus will obey the type of present cytosine in the injury site Thus, Th1 lymphocytes will have an associated phenotype to a cellular and proinflammatory answer, being that the Th2 lymphocytes will have an associated phenotype to a humoral and anti-inflammatory answer [7, 8]. …”

Section: Introductionmentioning

confidence: 99%

GAKG-RGEKG an Epitope That Provokes Immune Cross-Reactivity betweenPrevotellasp. and Human Collagen: Evidence of Molecular Mimicry in Chronic Periodontitis

Obando-Pereda

2016

Autoimmune Diseases

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Periodontal disease afflicts 20% of world population. This process usually occurs in the form of being lethargic and chronic, and consequently this disease is known as chronic process. All chronic diseases constantly cause activation of the immune system, and therefore the presentation of microbial peptides which are presented to lymphocytes by professional antigen presenting cells can present microbial peptides very similar to important structures of human economy causing autoimmune diseases, process known as molecular mimicry. Thus, the aim of this study was to verify the presence of molecular mimicry phenomenon between periodontopathogens and human proteins. Blasting microbes of Socransky periodontal complexes against human collagen were performed and then the proteins with similarities were modelled and were screened in the MHI binding virtual methods. The epitopes selected were produced and plasma of chronic periodontal volunteers was obtained and a dot immunobinding assay was performed. Hypothetical protein of Prevotella sp. and human collagen epitopes with high similarities were positive for dot immunobinding assay. With this result it can be suggested that the mimicry phenomena can occur on periodontal disease.

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Section: Introductionmentioning

confidence: 99%

GAKG-RGEKG an Epitope That Provokes Immune Cross-Reactivity betweenPrevotellasp. and Human Collagen: Evidence of Molecular Mimicry in Chronic Periodontitis

Obando-Pereda

2016

Autoimmune Diseases

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“…To further characterize differences between A/J, a low bone loss strain, and C57BL/6J, a high bone loss strain, tissue specimens were analyzed for immune and pro‐inflammatory cellular markers through immunohistochemistry (IHC) staining. Neutrophil and T cells were assessed in A/J and C57BL/6J mice after LPS treatment because neutrophils and T cells are known to infiltrate into periodontal lesions in response to infection and inflammation . When comparing control groups, there was no difference in immunostaining between C57BL/6J control and A/J control groups for both neutrophils and T cells.…”

Section: Resultsmentioning

confidence: 99%

Genomewide Association Study Identifies Cxcl Family Members as Partial Mediators of LPS-Induced Periodontitis

Hiyari

Green

Pan

et al. 2018

Journal of Bone and Mineral Research

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Periodontitis (PD) is characterized by bacterial infection and inflammation of tooth-supporting structures and can lead to tooth loss. PD affects ∼47% of the US population over age 30 years and has a heritability of about 50%. Although the host immunoinflammatory response and genetic background play a role, little is known of the underlying genetic factors. We examined natural genetic variation in lipopolysaccharide (LPS)-induced PD across a panel of inbred mouse strains, the hybrid mouse diversity panel (HMDP). We observed a strain-dependent sixfold difference in LPS-induced bone loss across the HMDP with a heritability of 53%. We performed a genomewide association study (GWAS) using FAST-LMM, which corrects for population structure, and identified loci significantly associated with PD. We examined candidate genes at a locus on chromosome 5, which suggested a relationship between LPS-induced bone loss and, together with expression data, identified Cxcl family members as associated with PD. We observed an increase in Cxcl10 protein, as well as immune cells and pro-inflammatory cytokines in C57BL/6J (high bone loss strain) but not in A/J (low bone loss strain) after LPS injections. Genetic deletion of CXCR3 (Cxcl9 and10 receptor) demonstrated a ∼50% reduction in bone loss and reduced osteoclasts after LPS injections. Furthermore, WT mice treated with AMG-487 (a CXCR3 antagonist) showed a ∼45% reduction in bone loss and decreased osteoclasts after LPS injections. We conclude that CXCR3 is a strong candidate for modulating the host response in individuals susceptible to PD. © 2018 American Society for Bone and Mineral Research.

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“…Studies have shown that some interleukins such as IL-10 reduce their levels during resolution of periodontitis (27). On the other hand, studies evaluating the immune response in the etiopathogenesis of periodontal diseases have evaluated that the development of media adaptive immunity by T lymphocytes that is highly dependent on antigen presenting cells associated to the innate immunity, where they produce different patterns of cytokines that will contribute to the polarization and activation of specific T lymphocytes (28).…”

Section: Discussionmentioning

confidence: 99%

Effects of Low Molecular Weight Heparin on Alveolar Bone Loss in Wistar Rats

et al. 2019

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This study aimed to assess the effects of low molecular weight heparin (LMWH) on alveolar bone loss (ABL), blood count, and counting of megakaryocytes and adipocytes in male Wistar rats. Forty male 60-day Wistar rats were randomly divided into four groups: Control (C), Periodontal Disease (PD), Heparin (Hp) and Heparin + Periodontal Disease (Hp+PD). LMWH was applied for 60 days at doses of 1 ml/kg/day. Blood samples were collected at baseline, 30 and 60. On day-49, PD and Hp+PD groups were subjected to ligature-induced periodontitis around second upper right molar. The left side was assessed as spontaneous alveolar bone loss. Mean ABL in the side with ligature showed significantly different between C (0.35±0.07 mm) and Hp+DP (0.49±0.09 mm) groups (p<0.001), between PD (0.55±0.11 mm) and Hp (0.32±0.06 mm) groups (p<0.001) and between Hp and Hp+DP groups (p<0.001). No significant differences were found among groups for ABL in the side without ligature. Animal weight, food intake, and water consumption showed no statistically significant difference among groups. Megakaryocytes and adipocytes were counted using optical microscopy and no statistically significant differences were found. Within-groups, there were an increase and a decrease, respectively, in the counting of lymphocytes (p=0.005 for C and p=0.009 for Hp+PD groups only) and leukocytes (p=0.003 for C, p=0.001 for PD, p=0.002 for Hp, and p<0.001 for Hp+PD groups). There was no decrease in the number of platelets in the three collection periods. LMWH was not able to affect ABL, but it may change the blood counting, especially increasing lymphocytes.

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T cells, teeth and tissue destruction – what do T cells do in periodontal disease?

Cited by 49 publications

References 88 publications

GAKG-RGEKG an Epitope That Provokes Immune Cross-Reactivity betweenPrevotellasp. and Human Collagen: Evidence of Molecular Mimicry in Chronic Periodontitis

GAKG-RGEKG an Epitope That Provokes Immune Cross-Reactivity betweenPrevotellasp. and Human Collagen: Evidence of Molecular Mimicry in Chronic Periodontitis

Genomewide Association Study Identifies Cxcl Family Members as Partial Mediators of LPS-Induced Periodontitis

Effects of Low Molecular Weight Heparin on Alveolar Bone Loss in Wistar Rats

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