T cells are able to promote lipopolysaccharide‐induced bone resorption in mice in the absence of B cells

Yamaguchi, Masahide; Ukai, Takashi; Kaneko, Takashi; Yoshinaga, M; Yokoyama, M; Hara, Yoshitaka

doi:10.1111/j.1600-0765.2008.01083.x

Cited by 25 publications

(19 citation statements)

References 36 publications

(70 reference statements)

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“…Still, the importance of these B cells in mediating alveolar bone loss is uncertain, as a considerable number of B cells was also found in mice without DT treatment, where no bone loss was observed. It was also demonstrated that B cells are not essential for LPS-induced bone loss, whereas T cells mediated this process (28). We, thus, argue that B cells might contribute to bone loss but are not crucial for this process.…”

Section: Discussionmentioning

confidence: 66%

Langerhans cells down-regulate inflammation-driven alveolar bone loss

Arizon

Nudel

Segev

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Excessive bone resorption is frequently associated with chronic infections and inflammatory diseases. Whereas T cells were demonstrated to facilitate osteoclastogenesis in such diseases, the role of dendritic cells, the most potent activators of naive T cells, remains unclear. Using a model involving inflammation-driven alveolar bone loss attributable to infection, we showed that in vivo ablation of Langerhans cells (LCs) resulted in enhanced bone loss. An increased infiltration of B and T lymphocytes into the tissue surrounding the bone was observed in LC-ablated mice, including receptor activator of NF-κB ligand (RANKL)-expressing CD4 + T cells with known capabilities of altering bone homeostasis. In addition, the absence of LCs significantly reduced the numbers of CD4 + Foxp3 + T-regulatory cells in the tissue. Further investigation revealed that LCs were not directly involved in presenting antigens to T cells. Nevertheless, despite their low numbers in the tissue, the absence of LCs resulted in an elevated activation of CD4 + but not CD8 + T cells. This activation involved elevated production of IFN-γ but not IL-17 or IL-10 cytokines. Our data, thus, reveal a protective immunoregulatory role for LCs in inflammation-induced alveolar bone resorption, by inhibiting IFN-γ secretion and excessive activation of RANKL + CD4 + T cells with a capability of promoting osteoclastogenesis.

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Section: Discussionmentioning

confidence: 66%

Langerhans cells down-regulate inflammation-driven alveolar bone loss

Arizon

Nudel

Segev

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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“…In animal models, mice deleted of B cells lack to develop bone loss when infected with P. gingivalis , even though B cells are dispensable. Indeed in absence of B cells, T cells still mediate LSP-induced bone loss [43]. …”

Section: Cytokines Involved In Bone Lossmentioning

confidence: 99%

Periodontal Disease: Linking the Primary Inflammation to Bone Loss

Benedetto

Gigante

Colucci

et al. 2013

Clinical and Developmental Immunology

250

249

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Periodontal disease (PD), or periodontitis, is defined as a bacterially induced disease of the tooth-supporting (periodontal) tissues. It is characterized by inflammation and bone loss; therefore understanding how they are linked would help to address the most efficacious therapeutic approach. Bacterial infection is the primary etiology but is not sufficient to induce the disease initiation or progression. Indeed, bacteria-derived factors stimulate a local inflammatory reaction and activation of the innate immune system. The innate response involves the recognition of microbial components by host cells, and this event is mediated by toll-like receptors (TLRs) expressed by resident cells and leukocytes. Activation of these cells leads to the release of proinflammatory cytokines and recruitment of phagocytes and lymphocytes. Activation of T and B cells initiates the adaptive immunity with Th1 Th2 Th17 Treg response and antibodies production respectively. In this inflammatory scenario, cytokines involved in bone regulation and maintenance have considerable relevance because tissue destruction is believed to be the consequence of host inflammatory response to the bacterial challenge. In the present review, we summarize host factors including cell populations, cytokines, and mechanisms involved in the destruction of the supporting tissues of the tooth and discuss treatment perspectives based on this knowledge.

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“…B-cells and T-cells are the main source of RANKL under these conditions [55]. Based on mouse models, T-cells are able to promote LPS-induced bone resorption in the absence of B-cells [56]. Basic research studies involving knockout of Pax-5, which is a transcription factor in B-cell development, show that massive osteoclastogenesis is another piece of the puzzle [57].…”

Section: B-cells and Bone Cells In Osteoimmunologymentioning

confidence: 98%

Cell biology of osteoimmunology

Gruber

2010

Wien Med Wochenschr

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Osteoimmunology is defined as the research area focusing on the crosstalk between the immune system and the muskoskeletal system. After nearly a decade of research, we are now beginning to understand the basic principles of this crosstalk. It seems that almost all immune cells are capable of communicating with osteoblasts, osteoclasts, and their respective progenitors - and vice versa. Diseases that fall into the category of osteoimmunology including osteoporosis, rheumatoid arthritis, and periodontal disease are of particular significance considering their implications in quality of life, their increased incidence in the population, and socioeconomic issues. To better understand the underlying pathogenesis, the main pathways of the crosstalk between the immune system and the muskoskeletal system need to be uncovered. Our current understanding has already provided the scientific basis for the development of targeted therapies. However, the challenge of future studies is to further decipher this crosstalk at cellular and molecular levels.

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T cells are able to promote lipopolysaccharide‐induced bone resorption in mice in the absence of B cells

Abstract: The results suggest that T cells are able to promote LPS-induced bone resorption in the absence of B cells. The expressions of cytokines in the presence of B cells are quite different.

Cited by 25 publications

References 36 publications

Langerhans cells down-regulate inflammation-driven alveolar bone loss

Langerhans cells down-regulate inflammation-driven alveolar bone loss

Periodontal Disease: Linking the Primary Inflammation to Bone Loss

Cell biology of osteoimmunology

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