The Experts below are selected from a list of 99 Experts worldwide ranked by ideXlab platform
Juan R. Velazquez - One of the best experts on this subject based on the ideXlab platform.
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Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes
Inflammation Research, 2010Co-Authors: Susana Godina-gonzalez, Janette Furuzawa-carballeda, Dolores Utrera-barillas, Jorge Alcocer-varela, Luis M. Teran, Monica Vazquez-del Mercado, Yelda A. Leal, Isabel Alvarado-cabrero, Juan R. VelazquezAbstract:Objective and design Monocyte locomotion inhibitory factor (MLIF), an amebic peptide with antiinflammatory properties, was evaluated in collagen-induced arthritis (CIA) to test its effects on the onset and acute inflammatory response of arthritis. Material DBA1/J mice at 8–10 weeks of age were divided into four groups (eight mice per group). Treatment The Adjuvant group received Freund Adjuvant, the CIA group was immunized with collagen II, the MLIF/CIA group received collagen II and MLIF, and the MLIF group received MLIF and Freund Adjuvant. Methods All groups were evaluated clinically. Seven weeks after the collagen injection, at the peak of the clinical arthritis score, limb specimens were collected and histological studies and gene expression analysis using microarrays were performed. Results MLIF administered weekly as a preventive scheme delayed and reduced the severity of acute arthritis. MLIF induced gene changes in functional categories including adhesion molecules, matrix metalloproteinases, and inflammatory cytokines. Conclusions MLIF could be an interesting new molecule to investigate in the field of rheumatoid arthritis pathogenesis research for its potential to prevent inflammation.
Hui Wang - One of the best experts on this subject based on the ideXlab platform.
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a myeloid cell population induced by Freund Adjuvant suppresses t cell mediated antitumor immunity
Journal of Immunotherapy, 2010Co-Authors: Zibing Wang, Jing Jiang, Zhiguang Li, Jinhua Zhang, Hui WangAbstract:Summary: Although Adjuvants are important components of vaccines, few studies have been conducted to establish the criteria on adju- vant selection and to investigate mechanisms of Adjuvant actions during vaccination. Here we found that complete Freund Adjuvant (CFA) induced a CD11b + cell population in a B-cell independent manner. This cell population exhibited strong ability to inhibit T-cellmediated rejection of tumor transplants. In vitro studies in- dicated that these cells induced T-cell apoptosis and down-regulated interferon-g production. Nitric oxide (NO) played important roles to achieve these effects. Plenty of NO was produced by these CFA- induced CD11b + cells. The addition of N G -nitro-L-arginine-methyl ester, an inhibitor of NO synthase, rescued T cells from apoptosis and partially abrogated the detrimental effects of CFA in cancer vaccines. Incomplete Freund Adjuvant, one of the Adjuvants still being used in clinical trials, also induced a similar cell population. Our results reveal a previously unknown mechanism in which the myeloid cell population induced by Freund Adjuvant impairs antitumor immu- nity, and highlight the importance of Adjuvant selection during tumor vaccination.
Patrick Matthys - One of the best experts on this subject based on the ideXlab platform.
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spect imaging of joint inflammation with nanobodies targeting the macrophage mannose receptor in a mouse model for rheumatoid arthritis
The Journal of Nuclear Medicine, 2013Co-Authors: Steve Schoonooghe, Nick Devoogdt, Evelien Schurgers, Anneleen Avau, Tania Mitera, Matthias Dhuyvetter, Patrick De Baetselier, Geert Raes, Tony Lahoutte, Patrick MatthysAbstract:Rheumatoid arthritis (RA) is a chronic autoimmune disease occurring in approximately 1% of the worldwide population. The disease primarily affects the joints, where inflammatory cells, such as macrophages, invade the synovium and cause cartilage and bone destruction. Currently, it is difficult to efficiently diagnose and monitor early-stage RA. In this study, we investigated whether SPECT/micro-CT imaging with 99mTclabeled Nanobodies directed against the macrophage mannose receptor (MMR) is a useful tool for monitoring and quantifying joint inflammation in collagen-induced arthritis (CIA), a mouse model for RA. The expression of MMR was analyzed on macrophages and osteoclasts generated in vitro and in cells obtained from various organs from mice with CIA. Methods: CIA was induced in DBA/1 mice by injection of collagen type II in complete Freund Adjuvant, and cell suspensions from the inflamed joints and other organs were obtained. Macrophages and osteoclasts were generated in vitro from bone marrow cells. Expression of MMR was quantified by quantitative polymerase chain reaction and flow cytometry with specific Nanobodies and conventional antibodies. SPECT/micro-CT imaging was performed with 99m Tc-labeled MMR and control Nanobodies. Results: MMR was highly expressed on macrophages and to a lesser extent on osteoclasts generated in vitro. In mice with CIA, MMR expression was detected on cells from the bone marrow, lymph nodes, and spleen. In synovial fluid of arthritic joints, MMR was expressed on CD11b1F4/801 macrophages. On in vivo SPECT/micro-CT imaging with consecutive injections of MMR and control Nanobodies, a strong MMR signal was seen in the knees, ankles, and toes of arthritic mice. Quantification of the SPECT imaging confirmed the specificity of the MMR signal in inflamed joints as compared with the control Nanobody. Dissection of the paws revealed an additional significant MMR signal in nonarthritic paws of affected mice (i.e., mice displaying symptoms of arthritis in other paws). Conclusion: Our data show that MMR is expressed on macrophages in vitro and in vivo in synovial fluid of inflamed paws, whereas expression is relatively low in other tissues. The use of Nanobodies against MMR in SPECT/micro-CT imaging generates the possibility to track inflammatory cells in vivo in arthritic joints.
P. Franchimont - One of the best experts on this subject based on the ideXlab platform.
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Endogenous production of specific antibodies does not decrease hypocalcemic response to calcitonin in young rabbits
Calcified Tissue International, 1992Co-Authors: Jean Yves Reginster, M. Azria, S. Gaspar, M. Bleicher, N. Franchimont, M. Behhar, A. Albert, P. FranchimontAbstract:In order to evaluate the potential inhibition of the acute anti-osteoclastic activity of salmon calcitonin (SCT) by specific antibodies (Ab), we compared the SCT-induced hypocalcemic effect in young male rabbits with significant titers of high affinity Ab and in matched animals without Ab. Immunization of rabbits was performed by repetitive s.c. injections of SCT and Freund Adjuvant. Ab were present in four-fifths of SCT-treated rabbits (Ab+). Their titer varied from 0.8×10(-9) to 30×10(-9) M/liter and their constant of affinity from 0.97×10(9) to 4.2×10(9) L/M. Intravenous injection of 1 IU/kg SCT to Ab+ rabbits induced a significant decrease ( P
Susana Godina-gonzalez - One of the best experts on this subject based on the ideXlab platform.
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Amebic monocyte locomotion inhibitory factor peptide ameliorates inflammation in CIA mouse model by downregulation of cell adhesion, inflammation/chemotaxis, and matrix metalloproteinases genes
Inflammation Research, 2010Co-Authors: Susana Godina-gonzalez, Janette Furuzawa-carballeda, Dolores Utrera-barillas, Jorge Alcocer-varela, Luis M. Teran, Monica Vazquez-del Mercado, Yelda A. Leal, Isabel Alvarado-cabrero, Juan R. VelazquezAbstract:Objective and design Monocyte locomotion inhibitory factor (MLIF), an amebic peptide with antiinflammatory properties, was evaluated in collagen-induced arthritis (CIA) to test its effects on the onset and acute inflammatory response of arthritis. Material DBA1/J mice at 8–10 weeks of age were divided into four groups (eight mice per group). Treatment The Adjuvant group received Freund Adjuvant, the CIA group was immunized with collagen II, the MLIF/CIA group received collagen II and MLIF, and the MLIF group received MLIF and Freund Adjuvant. Methods All groups were evaluated clinically. Seven weeks after the collagen injection, at the peak of the clinical arthritis score, limb specimens were collected and histological studies and gene expression analysis using microarrays were performed. Results MLIF administered weekly as a preventive scheme delayed and reduced the severity of acute arthritis. MLIF induced gene changes in functional categories including adhesion molecules, matrix metalloproteinases, and inflammatory cytokines. Conclusions MLIF could be an interesting new molecule to investigate in the field of rheumatoid arthritis pathogenesis research for its potential to prevent inflammation.
