The Experts below are selected from a list of 5673 Experts worldwide ranked by ideXlab platform
Joost J. Oppenheim - One of the best experts on this subject based on the ideXlab platform.
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autoantigens signal through chemokine receptors uveitis antigens induce cxcr3 and CXCR5 expressing lymphocytes and immature dendritic cells to migrate
Blood, 2005Co-Authors: O Zack M Howard, Hui Fang Dong, Shao Bo Su, Rachel R Caspi, Xin Chen, Paul H Plotz, Joost J. OppenheimAbstract:We tested the hypothesis that interaction between autoantigens and chemoattractant receptors may be an important step in the development of autoimmunity. The retinal autoantigens S-antigen (S-Ag) and interphotoreceptor retinoid binding protein (IRBP) can induce autoimmune uveitis in rodent models. We evaluated the chemotactic activity of S-Ag and IRBP and found that both induced migration of human and mouse immature dendritic cells (iDCs) and lymphocytes, but not neutrophils, monocytes, or mature DCs. Cross-desensitization studies and single-receptor transfected cells revealed that subfamily of alpha chemokine receptors CXCR5 and CXCR3 mediated the chemotactic effect of IRBP, while only CXCR3 was required for the chemotactic response to S-Ag. Examination of the relationships between chemoattraction and the ability to elicit pathology at the protein or peptide levels in the mouse uveitis model revealed dissociation of the capacity to induce uveitis, lymphocyte proliferation, and chemoattraction. These studies suggest that IRBP and S-Ag can initiate innate and, in sensitive individuals, adaptive immune response by attracting iDCs and T and B cells expressing CXCR3 and CXCR5.
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heterologous desensitization of opioid receptors by chemokines inhibits chemotaxis and enhances the perception of pain
Proceedings of the National Academy of Sciences of the United States of America, 2002Co-Authors: Imre Szabo, O M Z Howard, Martin W. Adler, Joost J. Oppenheim, Xiaohong Chen, Thomas J. RogersAbstract:The chemokines use G protein-coupled receptors to regulate the migratory and proadhesive responses of leukocytes. Based on observations that G protein-coupled receptors undergo heterologous desensitization, we have examined the ability of chemokines to also influence the perception of pain by cross-desensitizing opioid G protein-coupled receptors function in vitro and in vivo. We find that the chemotactic activities of both μ- and δ-opioid receptors are desensitized following activation of the chemokine receptors CCR5, CCR2, CCR7, and CXCR4 but not of the CXCR1 or CXCR2 receptors. Furthermore, we also find that pretreatment with RANTES/CCL5, the ligand for CCR1, and CCR5 or SDF-1α/CXCL12, the ligand for CXCR4, followed by opioid administration into the periaqueductal gray matter of the brain results in an increased rat tail flick response to a painful stimulus. Because chemokine administration into the periaqueductal gray matter inhibits opioid-induced analgesia, we propose that the activation of proinflammatory chemokine receptors down-regulates the analgesic functions of opioid receptors, and this enhances the perception of pain at inflammatory sites.
O Zack M Howard - One of the best experts on this subject based on the ideXlab platform.
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autoantigens signal through chemokine receptors uveitis antigens induce cxcr3 and CXCR5 expressing lymphocytes and immature dendritic cells to migrate
Blood, 2005Co-Authors: O Zack M Howard, Hui Fang Dong, Shao Bo Su, Rachel R Caspi, Xin Chen, Paul H Plotz, Joost J. OppenheimAbstract:We tested the hypothesis that interaction between autoantigens and chemoattractant receptors may be an important step in the development of autoimmunity. The retinal autoantigens S-antigen (S-Ag) and interphotoreceptor retinoid binding protein (IRBP) can induce autoimmune uveitis in rodent models. We evaluated the chemotactic activity of S-Ag and IRBP and found that both induced migration of human and mouse immature dendritic cells (iDCs) and lymphocytes, but not neutrophils, monocytes, or mature DCs. Cross-desensitization studies and single-receptor transfected cells revealed that subfamily of alpha chemokine receptors CXCR5 and CXCR3 mediated the chemotactic effect of IRBP, while only CXCR3 was required for the chemotactic response to S-Ag. Examination of the relationships between chemoattraction and the ability to elicit pathology at the protein or peptide levels in the mouse uveitis model revealed dissociation of the capacity to induce uveitis, lymphocyte proliferation, and chemoattraction. These studies suggest that IRBP and S-Ag can initiate innate and, in sensitive individuals, adaptive immune response by attracting iDCs and T and B cells expressing CXCR3 and CXCR5.
E Schmucking - One of the best experts on this subject based on the ideXlab platform.
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the role of CXCR5 and its ligand cxcl13 in the compartmentalization of lymphocytes in thyroids affected by autoimmune thyroid diseases
European Journal of Endocrinology, 2004Co-Authors: Gabriela Aust, D Sittig, L Becherer, U Anderegg, Alexander Schutz, P Lamesch, E SchmuckingAbstract:Objective: Graves' disease (GD) and Hashimoto's thyroiditis (HT) are characterized by lymphocytic infiltrates partly resembling secondary lymphoid follicles in the thyroid. CXCR5 and its ligand CXCL13 regulate compartmentalization of B- and T-cells in secondary lymphoid organs. The aim of the study was to elucidate the role of this chemokine receptor-ligand pair in thyroid autoimmunity. Methods: Peripheral blood and thyroid-derived lymphocyte subpopulations were examined by flow cytometry for CXCR5. CXCR5 and CXCL13 cDNA were quantified in thyroid tissues by real-time RT-PCR. Results: We found no differences between the percentages of peripheral blood CXCR5 + T- and B-cells in GD patients (n = 10) and healthy controls (n = 10). In GD patients, the number of memory CD4 + cells expressing CXCR 5 which are functionally characterized as follicular B helper T-cells is higher in thyroid-derived (18 ± 3%) compared with peripheral blood T-lymphocytes (8 ± 2%). The highest CXCL13 mRNA levels were found in HT (n = 2, 86.1 ± 1.2 zmol (10 -21 mol) cDNA/PCR) followed by GD tissues In = 16. 9.6 ± 3.5). Only low amounts were determined in thyroid autonomy (TA) (n = 11) thyroid tissues, irrespective ofwhether the autonomous nodule (0.5 ± 0.1) or the surrounding normal tissue (1.8 ± 0.7) had been analyzed. The same differences were found for CXCR 5 (HT: 1 79.1 ± 6.8; GD: 17.4 ± 10.6; TA nodule : 0.8±0.5; TA normal : 4.4±3.6). In GD. there is a correlation between CXCL13 and CXCR5 mRNA levels and the number of focal lymphocytic infiltrates and germinal centers as well as anti-thyroperoxidase but not anti-TSH receptor autoantibodies. Conclusions: CXCR and CXCL13 play an essential role in maintaining B- and T-cells in lymphocytic infiltrates and ectopic follicles in thyroid tissue from patients affected by autoimmunity.
Jianzhong Shen - One of the best experts on this subject based on the ideXlab platform.
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induction of c x c chemokine receptor type 7 cxcr7 switches stromal cell derived factor 1 sdf 1 signaling and phagocytic activity in macrophages linked to atherosclerosis
Journal of Biological Chemistry, 2013Co-Authors: Nicholas Ellison, Jianzhong ShenAbstract:The discovery of CXCR7 as a new receptor for SDF-1 places many previously described SDF-1 functions attributed to CXCR4 in question, though whether CXCR7 acts as a signaling or “decoy” receptor has been in debate. It is known that CXCR7 is not expressed in normal blood leukocytes; however, the potential role of leukocyte CXCR7 in disease states has not been addressed. The aim of this study was to determine the expression and function of macrophage CXCR7 linked to atherosclerosis. Here, we show that CXCR7 was detected in macrophage-positive area of aortic atheroma of ApoE-null mice, but not in healthy aorta. During monocyte differentiation to macrophages, CXCR7 was up-regulated at mRNA and protein levels, with more expression in M1 than in M2 phenotype. In addition, CXCR7 induction was associated with a SDF-1 signaling switch from the pro-survival ERK and AKT pathways in monocytes to the pro-inflammatory JNK and p38 pathways in macrophages. The latter effect was mimicked by a CXCR7-selective agonist TC14012 and abolished by siRNA knockdown of CXCR7. Furthermore, CXCR7 activation increased macrophage phagocytic activity, which was suppressed by CXCR7 siRNA silencing or by inhibiting either the JNK or p38 pathways, but was not affected by blocking CXCR4. Finally, activation of CXCR7 by I-TAC showed a similar signaling and phagocytic activity in macrophages with no detectable CXCR3. We conclude that CXCR7 is induced during monocyte-to-macrophage differentiation, which is required for SDF-1 and I-TAC signaling to JNK and p38 pathways, leading to enhanced macrophage phagocytosis, thus possibly contributing to atherogenesis.
Paul H Plotz - One of the best experts on this subject based on the ideXlab platform.
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to migrate cxcr3 and CXCR5 expressing lymphocytes and immature dendritic cells autoantigens signal through chemokine receptors uveitis antigens induce
2013Co-Authors: O M Howard, Hui Fang Dong, Shao Bo Su, Rachel R Caspi, Xin Chen, Paul H Plotz, J JoostAbstract:Abstract We tested the hypothesis that interaction between autoantigens and chemoattractant receptors may be an important step in the development of autoimmunity. The retinal autoantigens S-Antigen (S-Ag), and interphotoreceptor retinoid binding protein (IRBP) can induce autoimmune uveitis in rodent models. We evaluated the chemotactic activity of S-Ag and IRBP and found that both induced migration of human and mouse immature dendritic cells (iDCs) and lymphocytes, but not neutrophils, monocytes or mature DCs. Cross desensitization studies and single-receptor transfected cells revealed that CXCR5 and CXCR3 mediated the chemotactic effect of IRBP, while only CXCR3 was required for the chemotactic response to S-Ag. Examination of the relationships between chemoattraction and the ability to elicit pathology at the protein or peptide levels in the mouse uveitis model revealed dissociation of the capacity to induce uveitis, lymphocyte proliferation, and chemoattraction. These studies suggest that IRBP and S-Ag can initiate innate and, in sensitive individuals, adaptive immune response by attracting iDCs, T- and B-cells expressing CXCR3 and CXCR5. From bloodjournal.hematologylibrary.org by guest on June 1, 2013. For personal use only.
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autoantigens signal through chemokine receptors uveitis antigens induce cxcr3 and CXCR5 expressing lymphocytes and immature dendritic cells to migrate
Blood, 2005Co-Authors: O Zack M Howard, Hui Fang Dong, Shao Bo Su, Rachel R Caspi, Xin Chen, Paul H Plotz, Joost J. OppenheimAbstract:We tested the hypothesis that interaction between autoantigens and chemoattractant receptors may be an important step in the development of autoimmunity. The retinal autoantigens S-antigen (S-Ag) and interphotoreceptor retinoid binding protein (IRBP) can induce autoimmune uveitis in rodent models. We evaluated the chemotactic activity of S-Ag and IRBP and found that both induced migration of human and mouse immature dendritic cells (iDCs) and lymphocytes, but not neutrophils, monocytes, or mature DCs. Cross-desensitization studies and single-receptor transfected cells revealed that subfamily of alpha chemokine receptors CXCR5 and CXCR3 mediated the chemotactic effect of IRBP, while only CXCR3 was required for the chemotactic response to S-Ag. Examination of the relationships between chemoattraction and the ability to elicit pathology at the protein or peptide levels in the mouse uveitis model revealed dissociation of the capacity to induce uveitis, lymphocyte proliferation, and chemoattraction. These studies suggest that IRBP and S-Ag can initiate innate and, in sensitive individuals, adaptive immune response by attracting iDCs and T and B cells expressing CXCR3 and CXCR5.
