Joffre, O.; Gorsse, N.; Romagnoli, P.; Hudrisier, D.; van Meerwijk, J. P. M. Induction of antigen-specific tolerance to bone-marrow allografts with CD4+CD25+ T lymphocytes Journal Article In: Blood, vol. 103, no. 11, pp. 4216-4221, 2004. @article{RN118,
title = {Induction of antigen-specific tolerance to bone-marrow allografts with CD4+CD25+ T lymphocytes},
author = {Joffre, O. and Gorsse, N. and Romagnoli, P. and Hudrisier, D. and van Meerwijk, J. P.M.},
url = {file://D:%5CJoost's%20files%5Cmanuscripts%5CBlood%202004%20(Treg%20BM%20transplantation)%5CBlood%20submission%5Cresubmission%5CJoffre%20et%20al.pdf},
year = {2004},
date = {2004-01-01},
journal = {Blood},
volume = {103},
number = {11},
pages = {4216-4221},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
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Karim, Zoubida; Attmane-Elakeb, Amel; Sibella, Valérie; Bichara, Maurice Acid pH increases the stability of BSC1/NKCC2 mRNA in the medullary thick ascending limb Journal Article In: Journal of the American Society of Nephrology: JASN, vol. 14, no. 9, pp. 2229–2236, 2003, ISSN: 1046-6673. @article{karim_acid_2003,
title = {Acid pH increases the stability of BSC1/NKCC2 mRNA in the medullary thick ascending limb},
author = {Karim, Zoubida and Attmane-Elakeb, Amel and Sibella, Valérie and Bichara, Maurice},
doi = {10.1097/01.asn.0000085023.73801.4a},
issn = {1046-6673},
year = {2003},
date = {2003-09-01},
journal = {Journal of the American Society of Nephrology: JASN},
volume = {14},
number = {9},
pages = {2229--2236},
abstract = {Chronic metabolic acidosis enhances the ability of the medullary thick ascending limb (MTAL) to absorb NH(4)(+) at least in part by stimulating the mRNA and protein expression of BSC1/NKCC2, the MTAL apical Na(+)-K(+)(NH(4)(+))-2Cl(-) co-transporter. For assessing the mechanism by which an acid pH enhances the BSC1 mRNA abundance, MTAL were harvested from adrenalectomized rats and incubated in control (pH 7.35) and acid (pH 7.10) 1:1 mixtures of Ham's nutrient mixture F-12 and DME. rBSC1 mRNA abundance and gene transcription rate were quantified by quantitative reverse transcription-PCR and run-off assay, respectively. Acid incubation enhanced mRNA abundance within 4 h in whole cell (P textless 0.02) but not in nucleus. BSC1 gene transcription rate was not affected by acid incubation. In contrast, under conditions in which gene transcription was blocked, rBSC1 mRNA decreased within 6 h by 38 +/- 11% in control but only by 15 +/- 15% in acid medium (P textless 0.02), which represented an increase in the BSC1 mRNA half-life from approximately 7 to approximately 17 h. Furthermore, in a mouse TAL cell line, acid incubation for 16 h significantly increased (P textless 0.02) the amount of BSC1 mRNA in cells transfected with the full-length mBSC1 cDNA but not in cells transfected with a mBSC1 cDNA lacking the 3'-UTR. These results demonstrate that acid pH enhances the stability of BSC1 mRNA probably by activating pathways that act on the AU-rich 3'-UTR of BSC1 mRNA, which contributes to the renal response to metabolic acidosis.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Chronic metabolic acidosis enhances the ability of the medullary thick ascending limb (MTAL) to absorb NH(4)(+) at least in part by stimulating the mRNA and protein expression of BSC1/NKCC2, the MTAL apical Na(+)-K(+)(NH(4)(+))-2Cl(-) co-transporter. For assessing the mechanism by which an acid pH enhances the BSC1 mRNA abundance, MTAL were harvested from adrenalectomized rats and incubated in control (pH 7.35) and acid (pH 7.10) 1:1 mixtures of Ham's nutrient mixture F-12 and DME. rBSC1 mRNA abundance and gene transcription rate were quantified by quantitative reverse transcription-PCR and run-off assay, respectively. Acid incubation enhanced mRNA abundance within 4 h in whole cell (P textless 0.02) but not in nucleus. BSC1 gene transcription rate was not affected by acid incubation. In contrast, under conditions in which gene transcription was blocked, rBSC1 mRNA decreased within 6 h by 38 +/- 11% in control but only by 15 +/- 15% in acid medium (P textless 0.02), which represented an increase in the BSC1 mRNA half-life from approximately 7 to approximately 17 h. Furthermore, in a mouse TAL cell line, acid incubation for 16 h significantly increased (P textless 0.02) the amount of BSC1 mRNA in cells transfected with the full-length mBSC1 cDNA but not in cells transfected with a mBSC1 cDNA lacking the 3'-UTR. These results demonstrate that acid pH enhances the stability of BSC1 mRNA probably by activating pathways that act on the AU-rich 3'-UTR of BSC1 mRNA, which contributes to the renal response to metabolic acidosis. |
Capone, M.; Lees, R. L.; Finke, D.; Ernst, B.; van Meerwijk, J. P. M.; MacDonald, H. R. Selective absence of CD8+ TCRalpha beta+ intestinal epithelial cells in transgenic mice expressing beta2-microglobulin-associated ligands exclusively on thymic cortical epithelium. Journal Article In: Eur J Immunol, vol. 33, no. 6, pp. 1471-7, 2003. @article{RN114,
title = {Selective absence of CD8+ TCRalpha beta+ intestinal epithelial cells in transgenic mice expressing beta2-microglobulin-associated ligands exclusively on thymic cortical epithelium.},
author = {Capone, M. and Lees, R.L. and Finke, D. and Ernst, B. and van Meerwijk, J. P. M. and MacDonald, H. R.},
url = {D:Joost's filesarticlesCapone EJI 2003.pdf},
year = {2003},
date = {2003-01-01},
journal = {Eur J Immunol},
volume = {33},
number = {6},
pages = {1471-7},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Cemerski, S.; van Meerwijk, J. P. M.; Romagnoli, P. Oxidative stress-induced T lymphocyte hyporesponsiveness is caused by structural modification rather than proteasomal degradation of crucial signaling molecules Journal Article In: Eur J Immunol, vol. 33, no. 8, pp. 2178-85, 2003. @article{RN115,
title = {Oxidative stress-induced T lymphocyte hyporesponsiveness is caused by structural modification rather than proteasomal degradation of crucial signaling molecules},
author = {Cemerski, S. and van Meerwijk, J.P.M. and Romagnoli, P.},
year = {2003},
date = {2003-01-01},
journal = {Eur J Immunol},
volume = {33},
number = {8},
pages = {2178-85},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Hudrisier, D.; Feau, S.; Bonnet, V.; Romagnoli, P.; van Meerwijk, J. P. M. In vivo maintenance of T lymphocyte unresponsiveness induced by thymic medullary epithelium requires antigen presentation by radioresistant cells Journal Article In: Immunology, vol. 108, pp. 24-31, 2003. @article{RN108b,
title = {In vivo maintenance of T lymphocyte unresponsiveness induced by thymic medullary epithelium requires antigen presentation by radioresistant cells},
author = {Hudrisier, D. and Feau, S. and Bonnet, V. and Romagnoli, P. and van Meerwijk, J.P.M.},
year = {2003},
date = {2003-01-01},
journal = {Immunology},
volume = {108},
pages = {24-31},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Karim, Zoubida; Attmane-Elakeb, Amel; Bichara, Maurice Renal handling of NH4+ in relation to the control of acid-base balance by the kidney Journal Article In: Journal of Nephrology, vol. 15 Suppl 5, pp. S128–134, 2002, ISSN: 1121-8428. @article{karim_renal_2002,
title = {Renal handling of NH4+ in relation to the control of acid-base balance by the kidney},
author = {Karim, Zoubida and Attmane-Elakeb, Amel and Bichara, Maurice},
issn = {1121-8428},
year = {2002},
date = {2002-04-01},
journal = {Journal of Nephrology},
volume = {15 Suppl 5},
pages = {S128--134},
abstract = {The major component of urinary acid excretion is NH4+. To be appropriately excreted in urine, NH4+ must be synthesized by proximal tubular cells, secreted into the proximal tubular fluid, reabsorbed by the medullary thick ascending limb (MTAL) to be accumulated in the medullary interstitium, and finally secreted in medullary collecting ducts. Each step of this renal pathway is highly regulated and, in addition to acute events mediated by peptide hormones such as parathyroid hormone, the control of gene expression explains how the renal handling of NH4+ fully adapts to chronic changes in the acid-base status. Several targets have been identified at the gene expression level to account for the adaptation of renal NH4+ synthesis and transport in response to an acid load. These are the key enzymes of ammoniagenesis (mitochondrial glutaminase and glutamate dehydrogenase) and gluconeogenesis (phosphoenolpyruvate carboxykinase) in the proximal tubule, the apical Na(+)-K+(NH4+)-2Cl- cotransporter of the MTAL, and the basolateral Na(+)-K+(NH4+)-2Cl- cotransporter of medullary collecting ducts. At least two factors control the expression of these genes during metabolic acidosis: an acid pH and glucocorticoids, which appear to act in concert to coordinate the adaptation of various tubular cell types. The present review focuses on some aspects of these regulations that have been recently elucidated.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
The major component of urinary acid excretion is NH4+. To be appropriately excreted in urine, NH4+ must be synthesized by proximal tubular cells, secreted into the proximal tubular fluid, reabsorbed by the medullary thick ascending limb (MTAL) to be accumulated in the medullary interstitium, and finally secreted in medullary collecting ducts. Each step of this renal pathway is highly regulated and, in addition to acute events mediated by peptide hormones such as parathyroid hormone, the control of gene expression explains how the renal handling of NH4+ fully adapts to chronic changes in the acid-base status. Several targets have been identified at the gene expression level to account for the adaptation of renal NH4+ synthesis and transport in response to an acid load. These are the key enzymes of ammoniagenesis (mitochondrial glutaminase and glutamate dehydrogenase) and gluconeogenesis (phosphoenolpyruvate carboxykinase) in the proximal tubule, the apical Na(+)-K+(NH4+)-2Cl- cotransporter of the MTAL, and the basolateral Na(+)-K+(NH4+)-2Cl- cotransporter of medullary collecting ducts. At least two factors control the expression of these genes during metabolic acidosis: an acid pH and glucocorticoids, which appear to act in concert to coordinate the adaptation of various tubular cell types. The present review focuses on some aspects of these regulations that have been recently elucidated. |
Cemerski, S.; Cantagrel, A.; van Meerwijk, J. P. M.; Romagnoli, P. Reactive oxygen species differentially affect T cell receptor signaling pathways Journal Article In: Journal of Biological Chemistry, vol. 277, pp. 19585-19593, 2002. @article{RN106,
title = {Reactive oxygen species differentially affect T cell receptor signaling pathways},
author = {Cemerski, S. and Cantagrel, A. and van Meerwijk, J. P.M. and Romagnoli, P.},
url = {D:Joost's filesarticlesCemerski JBC 2002.pdf},
year = {2002},
date = {2002-01-01},
journal = {Journal of Biological Chemistry},
volume = {277},
pages = {19585-19593},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Constantin, A.; Lauwers-Cances, V.; Navaux, F.; Abbal, M.; van Meerwijk, J.; Mazieres, B.; Cambon-Thomsen, A.; Cantagrel, A. Collagenase-1 (MMP-1) and HLA-DRB1 gene polymorphisms in rheumatoid arthritis: a prospective longitudinal study Journal Article In: J Rheumatol, vol. 29, no. 1, pp. 15-20, 2002. @article{RN126,
title = {Collagenase-1 (MMP-1) and HLA-DRB1 gene polymorphisms in rheumatoid arthritis: a prospective longitudinal study},
author = {Constantin, A. and Lauwers-Cances, V. and Navaux, F. and Abbal, M. and van Meerwijk, J. and Mazieres, B. and Cambon-Thomsen, A. and Cantagrel, A.},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=11824952},
year = {2002},
date = {2002-01-01},
journal = {J Rheumatol},
volume = {29},
number = {1},
pages = {15-20},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Constantin, A.; Lauwers-Cances, V.; Navaux, F.; Abbal, M.; van Meerwijk, J.; Mazieres, B.; Cambon-Thomsen, A.; Cantagrel, A. Stromelysin 1 (matrix metalloproteinase 3) and HLA-DRB1 gene polymorphisms: Association with severity and progression of rheumatoid arthritis in a prospective study Journal Article In: Arthritis Rheum, vol. 46, no. 7, pp. 1754-62, 2002. @article{RN125,
title = {Stromelysin 1 (matrix metalloproteinase 3) and HLA-DRB1 gene polymorphisms: Association with severity and progression of rheumatoid arthritis in a prospective study},
author = {Constantin, A. and Lauwers-Cances, V. and Navaux, F. and Abbal, M. and van Meerwijk, J. and Mazieres, B. and Cambon-Thomsen, A. and Cantagrel, A.},
url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12124858},
year = {2002},
date = {2002-01-01},
journal = {Arthritis Rheum},
volume = {46},
number = {7},
pages = {1754-62},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Romagnoli, P.; Hudrisier, D.; van Meerwijk, J. P. M. Preferential recognition of self-antigens despite normal thymic deletion of CD4+CD25+ regulatory T cells Journal Article In: Journal of Immunology, vol. 168, pp. 1644-1648, 2002. @article{RN103,
title = {Preferential recognition of self-antigens despite normal thymic deletion of CD4+CD25+ regulatory T cells},
author = {Romagnoli, P. and Hudrisier, D. and van Meerwijk, J.P.M.},
url = {D:Joost's filesarticlesRomagnoli JI 2002.pdf},
year = {2002},
date = {2002-01-01},
journal = {Journal of Immunology},
volume = {168},
pages = {1644-1648},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Romagnoli, P.; Strahan, D.; Pelosi, M.; Cantagrel, A.; van Meerwijk, J. P. M. A potential role for tyrosine kinase p56lck in rheumatoid arthritis synovial fluid T lymphocyte hyporesponsiveness Journal Article In: International Immunology, vol. 13, no. 3, pp. 305-312, 2001. @article{RN91,
title = {A potential role for tyrosine kinase p56lck in rheumatoid arthritis synovial fluid T lymphocyte hyporesponsiveness},
author = {Romagnoli, P. and Strahan, D. and Pelosi, M. and Cantagrel, A. and van Meerwijk, J.P.M.},
year = {2001},
date = {2001-01-01},
journal = {International Immunology},
volume = {13},
number = {3},
pages = {305-312},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
|
Journal Article In: 0000. @article{noauthor_notitle_nodate,
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pubstate = {published},
tppubtype = {article}
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(No Title) Journal Article In: 0000. @article{d,
title = {(No Title)},
url = {http://science.sciencemag.org/},
doi = {10.1126/science.abf2022},
keywords = {},
pubstate = {published},
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[No title] Proceedings 0000. @proceedings{nokey,
title = {[No title]},
doi = {10.1038/s41582-019-0226-9},
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pubstate = {published},
tppubtype = {proceedings}
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