Augmented expression of tumour necrosis factor‐α induced by lipopolysaccharide in spleen of human monocyte chemoattractant protein‐1 transgenic mouse enhances the lipopolysaccharide sensitivity of the marginal zone macrophages

Ato, Manabu; Iwabuchi, Kazuya; Shimada, Shigeki; Mukaida, Naofumi; Onoé, Kazunori

doi:10.1046/j.1365-2567.2002.01450.x

Cited by 8 publications

(5 citation statements)

References 33 publications

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“…It is generally accepted that the expression of IL‐1 and TNF‐α might be induced by bacterial infection (30,31). Agents such as lipopolysaccharide interact with toll‐like receptors expressed on periodontal epithelial cells (32,33), which leads to periodontal disease. The epithelial cells of the mucosal surface, in addition to being able to form a mechanical barrier, can provide signals that are essential for the initiation and amplification of inflammatory responses during the course of bacterial infections.…”

Section: Discussionmentioning

confidence: 99%

Role of the junctional epithelium in periodontal innate defense and homeostasis

Usui

Yamamoto

et al. 2012

J of Periodontal Research

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Section: Discussionmentioning

confidence: 99%

Role of the junctional epithelium in periodontal innate defense and homeostasis

Usui

Yamamoto

et al. 2012

J of Periodontal Research

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“…37 Rat monoclonal antibodies (mAbs) to mouse macrophages (MOMA-2; Serotec, Oxford, United Kingdom), hamster antimouse CD3 (BD Biosciences, San Jose, CA), anti-␣-smooth muscle actin (DAKO, Glostrup, Denmark), rat antimouse IFN-␥ (BioSource), rat antimouse IL-10 (Endogen, Woburn, MA), biotinylated secondary antibodies to the respective primary reagents, and streptavidin-horseradish peroxidase (DAKO) were used for detection. Signals were developed with DBA kits (Vector Laboratories, Burlingame, CA).…”

Section: Characterization Of Atherosclerotic Lesionsmentioning

confidence: 99%

Natural killer T cells accelerate atherogenesis in mice

Nakai

Iwabuchi²,

Fujii³

et al. 2004

Blood

177

157

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In addition, repeated injections of ␣-GalCer or the related glycolipid OCH to apolipoprotein E knockout (apoE ؊/؊ ) mice during the early phase of atherosclerosis significantly enlarged the lesion areas compared with mice injected with vehicle control. However, administering ␣-GalCer to apoE ؊/؊ mice with established lesions did not significantly increase the lesion area but considerably decreased the collagen content. Atherosclerosis development in either AD-fed WT or apoE ؊/؊ mice was associated with the presence of V␣14J␣18 transcripts in the atherosclerotic arterial walls, indicating that NKT cells were recruited to these lesions. Thioglycolate-elicited macrophages pulsed with oxidized low-density lipoproteins expressed enhanced CD1d levels and induced NKT cells to produce interferon-␥, a potentially proatherogenic T-helper 1 (T H 1) cytokine. Collectively, we conclude that NKT cells are proatherogenic in mice. IntroductionAtherosclerosis is an inflammatory vascular disease that involves components of the innate and acquired immune systems. [1][2][3] Several studies have suggested that lymphocytes, which are detected in atherosclerotic lesions in humans and mice, 4,5 play a proatherogenic role. [6][7][8] Recently, the role of distinct lymphocyte subsets in the development of atherosclerosis has been evaluated. For example, emerging evidence indicates that T-helper 1 (T H 1) cells are proatherogenic, 9 whereas T H 2 cells are antiatherogenic. 10,11 These observations are further supported by the finding that T H 1 cytokines (eg,) are important in the progression of atherosclerosis [12][13][14][15] and that, among T H 2 cytokines, IL-10 is antiatherogenic. 16 On the other hand, recent studies have suggested that B cells play a protective role in atherogenesis. 17,18 Natural killer T (NKT) cells are a unique subset of lymphocytes that have surface markers and functions of T cells and NK cells. [19][20][21][22][23] Several characteristics of NKT cells suggest that they may play a role in the atherogenic process. Most NKT cells express an invariant V␣14J␣18 T-cell receptor (TCR)-V␣ chain paired with a restricted set of TCR-V␤ chains. These classical NKT cells recognize lipid antigens presented by the major histocompatibility complex (MHC) class 1-like molecule CD1d, produce copious amounts of IFN-␥ and IL-4 on activation, 22 and constitutively express Fas-ligand. 23 Moreover, NKT cells play a protective role in several autoimmune diseases, infections, and tumor progression/ metastasis. 20 Protective effects of NKT cells and their ligands in autoimmunity are largely attributed to their capacity to promote T H 2 immune responses. 24,25 However, in some situations, NKT cells can contribute to the development of T H 1 immune responses as well. 26 Therefore, it was difficult to predict whether NKT cells would play a proatherogenic or an antiatherogenic role. 2 To date, few studies have investigated the role of CD1d and CD1d-dependent T cells in atherogenesis. CD1d-expressing cells are present in human atherosclerotic...

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“…We also observed that Mer −/− macrophages (differentiated in vitro from BM cells or splenocytes) stimulated with ACs alone produced a twofold higher amount of the inflammatory cytokine TNFα compared to macrophages from WT mice challenged with ACs (Figure c–d). TNFα signaling is known to induce cell death in MZMs . Therefore, we reasoned that excessive production of TNFα due to impaired AC clearance in the splenic MZ in the absence of Mer could cause MZM dissipation.…”

Section: Resultsmentioning

confidence: 99%