Fractalkine in rheumatoid arthritis and allied conditions

Umehara, Hisanori; Tanaka, Masao; Sawaki, Toshioki; Jin, Zhe-Xiong; Huang, Cheng-Ri; Dong, Lingli; Kawanami, Takafumi; Karasawa, Hiromi; Yasukawa, Masaki; Fukushima, Toshihiro; Hirose, Yuko; Okazaki, Toshirou

doi:10.1007/s10165-006-0471-9

Cited by 20 publications

(19 citation statements)

References 48 publications

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“…Monocytes/macrophages, which play an important role as infiltrating cells at the site of inflammation, produce neopterin as well as the investigated chemokines CXCL13, CCL2, and CX3CL1 upon immune activation and stimulation by IFN-γ (19). Again chemokines are able to recruit and stimulate the infiltrating inflammatory cells to produce IFN-γ which stimulates the monocytes; CX3CL1 activates T-lymphocytes and NK cells, whereas CXCL13 addresses Band slightly T-cell activation (20).…”

Section: Resultsmentioning

confidence: 99%

Expression of Neopterin and Chemokines in Rheumatoid Arthritis and Cardiovascular Disease

Fagerer

Arnold²,

Bernatzky

et al. 2011

Pteridines

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In chronic inflammatory processes like rheumatoid arthritis (RA) and cardiovascular diseases (CVD) the role of pteridines and chemokines in the immune response is of great interest. The objectives of the study were to obtain information about an involvement of specific chemokines on the inflammatory process in patients with RA and CVD with activated production of the pteridine neopterin. 113 patients with RA according to American College of Rheumatology criteria including 24.8% suffering from CVD were included in the study (23% male, 77% female). For the assessment of monocyte activation and chemotaxis as well as the proinflammatory influence of chemokines on B-cells and angiogenesis in RA, neopterin and the chemokines CCL2, CXCL13 and CX3CL1 were measured by radio-and enzyme-immunoassays in serum. Neopterin and chemokines were all found in high concentrations. Neopterin significantly correlated with all chemokines: CXCL13 (r s = 0.368; p <0.0001), CX3CL1 (r s = 0.241; p <0.02), CCL2 (r s = 231; p <0.02), demonstrating high neopterin levels in RA patients to have a strong association to the chemokine induced chemotaxis of B-cells (CXCL13) and mononuclear cells (CX3CL1, CCL2). Significantly elevated concentrations of neopterin and CXCL13 were seen in patients with RA plus CVD compared to RA without CVD (p <0.03). The high incidence of cardiovascular diseases in rheumatoid arthritis seems to be associated with enhanced mononuclear (neopterin, CCL2) and B-cell activation (CXCL13), and as a consequence increased immune system activity.

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Section: Resultsmentioning

confidence: 99%

Expression of Neopterin and Chemokines in Rheumatoid Arthritis and Cardiovascular Disease

Fagerer

Arnold²,

Bernatzky

et al. 2011

Pteridines

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“…40 Moreover, CX 3 CR1 drives NK-cell migration toward inflamed tissues during multiple sclerosis 41 and rheumatoid arthritis. 42 Finally, CX 3 CR1 has a pivotal role in the recruitment of activated cytotoxic NK cells to the tumor. Indeed, defective antitumor responses detected in CX 3 CR1 Ϫ/Ϫ mice have been correlated with reduced NK-cell migration to the tumor microenvironment.…”

Section: Multiple Effects Of Soluble Hla-g On Nk Cells 5847mentioning

confidence: 99%

Soluble HLA-G dampens CD94/NKG2A expression and function and differentially modulates chemotaxis and cytokine and chemokine secretion in CD56bright and CD56dim NK cells

Morandi

Ferretti

Castriconi

et al. 2011

Blood

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Soluble HLA-G (sHLA-G) inhibits natural killer (NK) cell functions. Here, we investigated sHLA-G–mediated modulation of (1) chemokine receptor and NK receptor expression and function and (2) cytokine and chemokine secretion in CD56bright and CD56dim NK cells. sHLA-G-treated or untreated peripheral blood (PB) and tonsil NK cells were analyzed for chemokine receptor and NK receptor expression by flow cytometry. sHLA-G down-modulated (1) CXCR3 on PB and tonsil CD56bright and CD56dim, (2) CCR2 on PB and tonsil CD56bright, (3) CX3CR1 on PB CD56dim, (4) CXCR5 on tonsil CD56dim, and (5) CD94/NKG2A on PB and tonsil CD56bright and CD56dim NK cells. Such sHLA-G–mediated down-modulations were reverted by adding anti–HLA-G or anti–ILT2 mAbs. sHLA-G inhibited chemotaxis of (1) PB NK cells toward CXCL10, CXCL11, and CX3CL1 and (2) PB CD56bright NK cells toward CCL2 and CXCL10. IFN-γ secretion induced by NKp46 engagement was inhibited by NKG2A engagement in untreated but not in sHLA-G–treated NK cells. sHLA-G up-regulated secretion of (1) CCL22 in CD56bright and CD56dim and (2) CCL2, CCL8, and CXCL2-CXCL3 in CD56dim PB NK cells. Signal transduction experiments showed sHLA-G–mediated down-modulation of Stat5 phosphorylation in PB NK cells. In conclusion, our data delineated novel mechanisms of sHLA-G–mediated inhibition of NK-cell functions.

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“…[126][127][128] High levels of fractalkine and its receptor are expressed at wound sites. 114,129 In vitro, fractalkine stimulated chemotaxis by MIP, macrophage inflammatory protein; RANTES, regulated on activation normal T-cell expressed and secreted; MCP, monocyte chemoattractant protein; TARC, thymus and activation-regulated chemokine; MDC, macrophage-derived chemokine; SLC, secondary lymphoid tissue chemokine; IL, interleukin; SDF, stromal cell derived factor.…”

Section: Fractalkinementioning

confidence: 99%

In SituTissue Regeneration: Chemoattractants for Endogenous Stem Cell Recruitment

Berg-Foels

2014

Tissue Engineering Part B: Reviews

132

111

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Tissue engineering uses cells, signaling molecules, and/or biomaterials to regenerate injured or diseased tissues. Ex vivo expanded mesenchymal stem cells (MSC) have long been a cornerstone of regeneration therapies; however, drawbacks that include altered signaling responses and reduced homing capacity have prompted investigation of regeneration based on endogenous MSC recruitment. Recent successful proof-of-concept studies have further motivated endogenous MSC recruitment-based approaches. Stem cell migration is required for morphogenesis and organogenesis during development and for tissue maintenance and injury repair in adults. A biomimetic approach to in situ tissue regeneration by endogenous MSC requires the orchestration of three main stages: MSC recruitment, MSC differentiation, and neotissue maturation. The first stage must result in recruitment of a sufficient number of MSC, capable of effecting regeneration, to the injured or diseased tissue. One of the challenges for engineering endogenous MSC recruitment is the selection of effective chemoattractant(s). The objective of this review is to synthesize and evaluate evidence of recruitment efficacy by reported chemoattractants, including growth factors, chemokines, and other more recently appreciated MSC chemoattractants. The influence of MSC tissue sources, cell culture methods, and the in vitro and in vivo environments is discussed. This growing body of knowledge will serve as a basis for the rational design of regenerative therapies based on endogenous MSC recruitment. Successful endogenous MSC recruitment is the first step of successful tissue regeneration

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Fractalkine in rheumatoid arthritis and allied conditions

Cited by 20 publications

References 48 publications

Expression of Neopterin and Chemokines in Rheumatoid Arthritis and Cardiovascular Disease

Expression of Neopterin and Chemokines in Rheumatoid Arthritis and Cardiovascular Disease

Soluble HLA-G dampens CD94/NKG2A expression and function and differentially modulates chemotaxis and cytokine and chemokine secretion in CD56bright and CD56dim NK cells

In SituTissue Regeneration: Chemoattractants for Endogenous Stem Cell Recruitment

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