The Experts below are selected from a list of 3078 Experts worldwide ranked by ideXlab platform
Jun Wada - One of the best experts on this subject based on the ideXlab platform.
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cerebroside sulfotransferase deficiency ameliorates l selectin dependent monocyte infiltration in the Kidney after ureteral obstruction
Journal of Biological Chemistry, 2004Co-Authors: Daisuke Ogawa, Koichi Honke, Kenichi Shikata, Shinichi Sato, Mitsuhiro Matsuda, Ryo Nagase, Atsuhito Tone, Shinichi Okada, Hitomi Usui, Jun WadaAbstract:Abstract Mononuclear cells infiltrating the Interstitium are involved in renal tubulointerstitial injury. The unilateral ureteral obstruction (UUO) is an established experimental model of renal interstitial inflammation. In our previous study, we postulated that L-selectin on monocytes is involved in their infiltration into the Interstitium by UUO and that a sulfated glycolipid, sulfatide, is the physiological L-selectin ligand in the Kidney. Here we tested the above hypothesis using sulfatide- and L-selectin-deficient mice. Sulfatide-deficient mice were generated by gene targeting of the cerebroside sulfotransferase (Cst) gene. Although the L-selectin-IgG chimera protein specifically bound to sulfatide fraction in acidic lipids from wild-type Kidney, it did not show such binding in fractions of Cst-/- mice Kidney, indicating that sulfatide is the major L-selectin-binding glycolipid in the Kidney. The distribution of L-selectin ligand in wild-type mice changed after UUO; sulfatide was relocated from the distal tubules to the peritubular capillaries where monocytes infiltrate, suggesting that sulfatide relocated to the endothelium after UUO interacted with L-selectin on monocytes. In contrast, L-selectin ligand was not detected in Cst-/- mice irrespective of UUO treatment. Compared with wild-type mice, Cst-/- mice showed a considerable reduction in the number of monocytes/macrophages that infiltrated the Interstitium after UUO. The number of monocytes/macrophages was also reduced to a similar extent in L-selectin-/- mice. Our results suggest that sulfatide is a major L-selectin-binding molecule in the Kidney and that the interaction between L-selectin and sulfatide plays a critical role in monocyte infiltration into the Kidney Interstitium.
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l selectin and its ligands mediate infiltration of mononuclear cells into Kidney Interstitium after ureteric obstruction
The Journal of Pathology, 1999Co-Authors: Kenichi Shikata, Mitsuhiro Matsuda, Jun Wada, Kyoji Hirata, Hirofumi Makino, Yasuo Suzuki, Hiroto Kawashima, Takashi Suzuki, Masako Iizuka, Masayuki MiyasakaAbstract:It was previously reported that the L-selectin ligands detected by a rat L-selectin and human IgG chimeric molecule (rLEC-IgG) are expressed in the distal tubules of the Kidney, where no leukocyte traffic is seen under physiological conditions. In the present study, the role of L-selectin ligands in leukocyte infiltration into the Kidney Interstitium was investigated using a rat ureteric obstruction model. After ligation of the ureter, ligands for L-selectin rapidly disappeared from tubular epithelial cells and were relocated to the Interstitium and peritubular capillary walls, where infiltration of monocytes and CD8(+) T cells subsequently occurred. Mononuclear cell infiltration was significantly inhibited by intravenous injection of a neutralizing monoclonal antibody (MAb) against L-selectin, indicating the possible involvement of an L-selectin-mediated pathway. Interestingly, immunohistochemical studies with a MAb against sulphatide showed that the distribution of sulphatide, known to be one of the candidates of L-selectin ligand, was almost indistinguishable from the staining pattern of rLEC-IgG in both normal and ureteric obstructed Kidneys, suggesting that sulphatide and/or related molecule(s) relocated to the renal Interstitium were recognized by leukocyte L-selectin, leading to interstitial leukocyte infiltration. In line with this notion, intravenous injection of sulphatide markedly inhibited leukocyte infiltration, suggesting that L-selectin-sulphatide interaction may play a pivotal role in interstitial leukocyte infiltration in the Kidney following ureteric obstruction.
Pierre Aucouturier - One of the best experts on this subject based on the ideXlab platform.
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Evidence of follicular T-cell implication in a case of IgG4-related systemic disease with interstitial nephritis
Nephrology Dialysis Transplantation, 2011Co-Authors: Mohamad Zaidan, Pascale Cervera-pierot, Sophie De Seigneux, Karine Dahan, Bettina Fabiani, Patrice Callard, Pierre Ronco, Pierre AucouturierAbstract:: IgG4-related systemic disease is a protean disorder that covers a wide variety of lesions. We report on a patient with tubulointerstitial nephritis, lymphadenopathies, sialadenitis and retroperitoneal fibrosis. The salivary gland and Kidney Interstitium were infiltrated with B lymphocytes and T lymphocytes and IgG3(+) and IgG4(+) plasma cells. The overexpression of IgG1 and IgG3, in addition to IgG4, the unusual abundance of interfollicular plasma cells and CD4(+) T cells in germinal centres of lymph nodes, and the dramatic response to rituximab point to possible roles of follicular helper T cells in enhancing a skewed B-cell terminal maturation and of CD20(+) B cells in disease progression.
Kenichi Shikata - One of the best experts on this subject based on the ideXlab platform.
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cerebroside sulfotransferase deficiency ameliorates l selectin dependent monocyte infiltration in the Kidney after ureteral obstruction
Journal of Biological Chemistry, 2004Co-Authors: Daisuke Ogawa, Koichi Honke, Kenichi Shikata, Shinichi Sato, Mitsuhiro Matsuda, Ryo Nagase, Atsuhito Tone, Shinichi Okada, Hitomi Usui, Jun WadaAbstract:Abstract Mononuclear cells infiltrating the Interstitium are involved in renal tubulointerstitial injury. The unilateral ureteral obstruction (UUO) is an established experimental model of renal interstitial inflammation. In our previous study, we postulated that L-selectin on monocytes is involved in their infiltration into the Interstitium by UUO and that a sulfated glycolipid, sulfatide, is the physiological L-selectin ligand in the Kidney. Here we tested the above hypothesis using sulfatide- and L-selectin-deficient mice. Sulfatide-deficient mice were generated by gene targeting of the cerebroside sulfotransferase (Cst) gene. Although the L-selectin-IgG chimera protein specifically bound to sulfatide fraction in acidic lipids from wild-type Kidney, it did not show such binding in fractions of Cst-/- mice Kidney, indicating that sulfatide is the major L-selectin-binding glycolipid in the Kidney. The distribution of L-selectin ligand in wild-type mice changed after UUO; sulfatide was relocated from the distal tubules to the peritubular capillaries where monocytes infiltrate, suggesting that sulfatide relocated to the endothelium after UUO interacted with L-selectin on monocytes. In contrast, L-selectin ligand was not detected in Cst-/- mice irrespective of UUO treatment. Compared with wild-type mice, Cst-/- mice showed a considerable reduction in the number of monocytes/macrophages that infiltrated the Interstitium after UUO. The number of monocytes/macrophages was also reduced to a similar extent in L-selectin-/- mice. Our results suggest that sulfatide is a major L-selectin-binding molecule in the Kidney and that the interaction between L-selectin and sulfatide plays a critical role in monocyte infiltration into the Kidney Interstitium.
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l selectin and its ligands mediate infiltration of mononuclear cells into Kidney Interstitium after ureteric obstruction
The Journal of Pathology, 1999Co-Authors: Kenichi Shikata, Mitsuhiro Matsuda, Jun Wada, Kyoji Hirata, Hirofumi Makino, Yasuo Suzuki, Hiroto Kawashima, Takashi Suzuki, Masako Iizuka, Masayuki MiyasakaAbstract:It was previously reported that the L-selectin ligands detected by a rat L-selectin and human IgG chimeric molecule (rLEC-IgG) are expressed in the distal tubules of the Kidney, where no leukocyte traffic is seen under physiological conditions. In the present study, the role of L-selectin ligands in leukocyte infiltration into the Kidney Interstitium was investigated using a rat ureteric obstruction model. After ligation of the ureter, ligands for L-selectin rapidly disappeared from tubular epithelial cells and were relocated to the Interstitium and peritubular capillary walls, where infiltration of monocytes and CD8(+) T cells subsequently occurred. Mononuclear cell infiltration was significantly inhibited by intravenous injection of a neutralizing monoclonal antibody (MAb) against L-selectin, indicating the possible involvement of an L-selectin-mediated pathway. Interestingly, immunohistochemical studies with a MAb against sulphatide showed that the distribution of sulphatide, known to be one of the candidates of L-selectin ligand, was almost indistinguishable from the staining pattern of rLEC-IgG in both normal and ureteric obstructed Kidneys, suggesting that sulphatide and/or related molecule(s) relocated to the renal Interstitium were recognized by leukocyte L-selectin, leading to interstitial leukocyte infiltration. In line with this notion, intravenous injection of sulphatide markedly inhibited leukocyte infiltration, suggesting that L-selectin-sulphatide interaction may play a pivotal role in interstitial leukocyte infiltration in the Kidney following ureteric obstruction.
Mitsuhiro Matsuda - One of the best experts on this subject based on the ideXlab platform.
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cerebroside sulfotransferase deficiency ameliorates l selectin dependent monocyte infiltration in the Kidney after ureteral obstruction
Journal of Biological Chemistry, 2004Co-Authors: Daisuke Ogawa, Koichi Honke, Kenichi Shikata, Shinichi Sato, Mitsuhiro Matsuda, Ryo Nagase, Atsuhito Tone, Shinichi Okada, Hitomi Usui, Jun WadaAbstract:Abstract Mononuclear cells infiltrating the Interstitium are involved in renal tubulointerstitial injury. The unilateral ureteral obstruction (UUO) is an established experimental model of renal interstitial inflammation. In our previous study, we postulated that L-selectin on monocytes is involved in their infiltration into the Interstitium by UUO and that a sulfated glycolipid, sulfatide, is the physiological L-selectin ligand in the Kidney. Here we tested the above hypothesis using sulfatide- and L-selectin-deficient mice. Sulfatide-deficient mice were generated by gene targeting of the cerebroside sulfotransferase (Cst) gene. Although the L-selectin-IgG chimera protein specifically bound to sulfatide fraction in acidic lipids from wild-type Kidney, it did not show such binding in fractions of Cst-/- mice Kidney, indicating that sulfatide is the major L-selectin-binding glycolipid in the Kidney. The distribution of L-selectin ligand in wild-type mice changed after UUO; sulfatide was relocated from the distal tubules to the peritubular capillaries where monocytes infiltrate, suggesting that sulfatide relocated to the endothelium after UUO interacted with L-selectin on monocytes. In contrast, L-selectin ligand was not detected in Cst-/- mice irrespective of UUO treatment. Compared with wild-type mice, Cst-/- mice showed a considerable reduction in the number of monocytes/macrophages that infiltrated the Interstitium after UUO. The number of monocytes/macrophages was also reduced to a similar extent in L-selectin-/- mice. Our results suggest that sulfatide is a major L-selectin-binding molecule in the Kidney and that the interaction between L-selectin and sulfatide plays a critical role in monocyte infiltration into the Kidney Interstitium.
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l selectin and its ligands mediate infiltration of mononuclear cells into Kidney Interstitium after ureteric obstruction
The Journal of Pathology, 1999Co-Authors: Kenichi Shikata, Mitsuhiro Matsuda, Jun Wada, Kyoji Hirata, Hirofumi Makino, Yasuo Suzuki, Hiroto Kawashima, Takashi Suzuki, Masako Iizuka, Masayuki MiyasakaAbstract:It was previously reported that the L-selectin ligands detected by a rat L-selectin and human IgG chimeric molecule (rLEC-IgG) are expressed in the distal tubules of the Kidney, where no leukocyte traffic is seen under physiological conditions. In the present study, the role of L-selectin ligands in leukocyte infiltration into the Kidney Interstitium was investigated using a rat ureteric obstruction model. After ligation of the ureter, ligands for L-selectin rapidly disappeared from tubular epithelial cells and were relocated to the Interstitium and peritubular capillary walls, where infiltration of monocytes and CD8(+) T cells subsequently occurred. Mononuclear cell infiltration was significantly inhibited by intravenous injection of a neutralizing monoclonal antibody (MAb) against L-selectin, indicating the possible involvement of an L-selectin-mediated pathway. Interestingly, immunohistochemical studies with a MAb against sulphatide showed that the distribution of sulphatide, known to be one of the candidates of L-selectin ligand, was almost indistinguishable from the staining pattern of rLEC-IgG in both normal and ureteric obstructed Kidneys, suggesting that sulphatide and/or related molecule(s) relocated to the renal Interstitium were recognized by leukocyte L-selectin, leading to interstitial leukocyte infiltration. In line with this notion, intravenous injection of sulphatide markedly inhibited leukocyte infiltration, suggesting that L-selectin-sulphatide interaction may play a pivotal role in interstitial leukocyte infiltration in the Kidney following ureteric obstruction.
Mohamad Zaidan - One of the best experts on this subject based on the ideXlab platform.
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Evidence of follicular T-cell implication in a case of IgG4-related systemic disease with interstitial nephritis
Nephrology Dialysis Transplantation, 2011Co-Authors: Mohamad Zaidan, Pascale Cervera-pierot, Sophie De Seigneux, Karine Dahan, Bettina Fabiani, Patrice Callard, Pierre Ronco, Pierre AucouturierAbstract:: IgG4-related systemic disease is a protean disorder that covers a wide variety of lesions. We report on a patient with tubulointerstitial nephritis, lymphadenopathies, sialadenitis and retroperitoneal fibrosis. The salivary gland and Kidney Interstitium were infiltrated with B lymphocytes and T lymphocytes and IgG3(+) and IgG4(+) plasma cells. The overexpression of IgG1 and IgG3, in addition to IgG4, the unusual abundance of interfollicular plasma cells and CD4(+) T cells in germinal centres of lymph nodes, and the dramatic response to rituximab point to possible roles of follicular helper T cells in enhancing a skewed B-cell terminal maturation and of CD20(+) B cells in disease progression.
