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  • 1
    Publication Date: 2008-08-22
    Description: Interleukin (IL)-17-producing CD4(+) T lymphocytes (T(H)17 cells) constitute a subset of T-helper cells involved in host defence and several immune disorders. An intriguing feature of T(H)17 cells is their selective and constitutive presence in the intestinal lamina propria. Here we show that adenosine 5'-triphosphate (ATP) that can be derived from commensal bacteria activates a unique subset of lamina propria cells, CD70(high)CD11c(low) cells, leading to the differentiation of T(H)17 cells. Germ-free mice exhibit much lower concentrations of luminal ATP, accompanied by fewer lamina propria T(H)17 cells, compared to specific-pathogen-free mice. Systemic or rectal administration of ATP into these germ-free mice results in a marked increase in the number of lamina propria T(H)17 cells. A CD70(high)CD11c(low) subset of the lamina propria cells expresses T(H)17-prone molecules, such as IL-6, IL-23p19 and transforming-growth-factor-beta-activating integrin-alphaV and -beta8, in response to ATP stimulation, and preferentially induces T(H)17 differentiation of co-cultured naive CD4(+) T cells. The critical role of ATP is further underscored by the observation that administration of ATP exacerbates a T-cell-mediated colitis model with enhanced T(H)17 differentiation. These observations highlight the importance of commensal bacteria and ATP for T(H)17 differentiation in health and disease, and offer an explanation of why T(H)17 cells specifically present in the intestinal lamina propria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Atarashi, Koji -- Nishimura, Junichi -- Shima, Tatsuichiro -- Umesaki, Yoshinori -- Yamamoto, Masahiro -- Onoue, Masaharu -- Yagita, Hideo -- Ishii, Naoto -- Evans, Richard -- Honda, Kenya -- Takeda, Kiyoshi -- England -- Nature. 2008 Oct 9;455(7214):808-12. doi: 10.1038/nature07240. Epub 2008 Aug 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immune Regulation, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18716618" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism/*pharmacology ; Animals ; Antigens, CD11c/metabolism ; Antigens, CD70/metabolism ; Cell Differentiation/*drug effects ; Cells, Cultured ; Colitis/chemically induced/immunology/pathology ; Disease Models, Animal ; Feces/microbiology ; Female ; Germ-Free Life ; Immunoglobulin A/analysis/immunology ; Interleukin-17/genetics/immunology/metabolism ; Male ; Mice ; Mucous Membrane/*cytology/*drug effects/immunology/microbiology ; Receptors, Purinergic P2/metabolism ; T-Lymphocytes, Helper-Inducer/*cytology/*drug effects/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2009-07-22
    Description: Acquired uniparental disomy (aUPD) is a common feature of cancer genomes, leading to loss of heterozygosity. aUPD is associated not only with loss-of-function mutations of tumour suppressor genes, but also with gain-of-function mutations of proto-oncogenes. Here we show unique gain-of-function mutations of the C-CBL (also known as CBL) tumour suppressor that are tightly associated with aUPD of the 11q arm in myeloid neoplasms showing myeloproliferative features. The C-CBL proto-oncogene, a cellular homologue of v-Cbl, encodes an E3 ubiquitin ligase and negatively regulates signal transduction of tyrosine kinases. Homozygous C-CBL mutations were found in most 11q-aUPD-positive myeloid malignancies. Although the C-CBL mutations were oncogenic in NIH3T3 cells, c-Cbl was shown to functionally and genetically act as a tumour suppressor. C-CBL mutants did not have E3 ubiquitin ligase activity, but inhibited that of wild-type C-CBL and CBL-B (also known as CBLB), leading to prolonged activation of tyrosine kinases after cytokine stimulation. c-Cbl(-/-) haematopoietic stem/progenitor cells (HSPCs) showed enhanced sensitivity to a variety of cytokines compared to c-Cbl(+/+) HSPCs, and transduction of C-CBL mutants into c-Cbl(-/-) HSPCs further augmented their sensitivities to a broader spectrum of cytokines, including stem-cell factor (SCF, also known as KITLG), thrombopoietin (TPO, also known as THPO), IL3 and FLT3 ligand (FLT3LG), indicating the presence of a gain-of-function that could not be attributed to a simple loss-of-function. The gain-of-function effects of C-CBL mutants on cytokine sensitivity of HSPCs largely disappeared in a c-Cbl(+/+) background or by co-transduction of wild-type C-CBL, which suggests the pathogenic importance of loss of wild-type C-CBL alleles found in most cases of C-CBL-mutated myeloid neoplasms. Our findings provide a new insight into a role of gain-of-function mutations of a tumour suppressor associated with aUPD in the pathogenesis of some myeloid cancer subsets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanada, Masashi -- Suzuki, Takahiro -- Shih, Lee-Yung -- Otsu, Makoto -- Kato, Motohiro -- Yamazaki, Satoshi -- Tamura, Azusa -- Honda, Hiroaki -- Sakata-Yanagimoto, Mamiko -- Kumano, Keiki -- Oda, Hideaki -- Yamagata, Tetsuya -- Takita, Junko -- Gotoh, Noriko -- Nakazaki, Kumi -- Kawamata, Norihiko -- Onodera, Masafumi -- Nobuyoshi, Masaharu -- Hayashi, Yasuhide -- Harada, Hiroshi -- Kurokawa, Mineo -- Chiba, Shigeru -- Mori, Hiraku -- Ozawa, Keiya -- Omine, Mitsuhiro -- Hirai, Hisamaru -- Nakauchi, Hiromitsu -- Koeffler, H Phillip -- Ogawa, Seishi -- 2R01CA026038-30/CA/NCI NIH HHS/ -- England -- Nature. 2009 Aug 13;460(7257):904-8. doi: 10.1038/nature08240. Epub 2009 Jul 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genomics Project, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19620960" target="_blank"〉PubMed〈/a〉
    Keywords: Allelic Imbalance ; Amino Acid Sequence ; Animals ; Base Sequence ; Chromosomes, Human, Pair 11/genetics ; Female ; *Genes, Tumor Suppressor ; Humans ; Leukemia, Myeloid/*genetics/metabolism/pathology ; Male ; Mice ; Mice, Knockout ; Mice, Nude ; Models, Molecular ; Molecular Sequence Data ; Mutant Proteins/chemistry/genetics/*metabolism ; Mutation ; NIH 3T3 Cells ; Neoplasm Transplantation ; Oncogenes/genetics ; Phosphorylation ; Protein Conformation ; Proto-Oncogene Proteins c-cbl/antagonists & ; inhibitors/chemistry/deficiency/*genetics/*metabolism ; Ubiquitination ; Uniparental Disomy/genetics ; ras Proteins/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2005-09-10
    Description: On 4 July 2005, many observatories around the world and in space observed the collision of Deep Impact with comet 9P/Tempel 1 or its aftermath. This was an unprecedented coordinated observational campaign. These data show that (i) there was new material after impact that was compositionally different from that seen before impact; (ii) the ratio of dust mass to gas mass in the ejecta was much larger than before impact; (iii) the new activity did not last more than a few days, and by 9 July the comet's behavior was indistinguishable from its pre-impact behavior; and (iv) there were interesting transient phenomena that may be correlated with cratering physics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meech, K J -- Ageorges, N -- A'Hearn, M F -- Arpigny, C -- Ates, A -- Aycock, J -- Bagnulo, S -- Bailey, J -- Barber, R -- Barrera, L -- Barrena, R -- Bauer, J M -- Belton, M J S -- Bensch, F -- Bhattacharya, B -- Biver, N -- Blake, G -- Bockelee-Morvan, D -- Boehnhardt, H -- Bonev, B P -- Bonev, T -- Buie, M W -- Burton, M G -- Butner, H M -- Cabanac, R -- Campbell, R -- Campins, H -- Capria, M T -- Carroll, T -- Chaffee, F -- Charnley, S B -- Cleis, R -- Coates, A -- Cochran, A -- Colom, P -- Conrad, A -- Coulson, I M -- Crovisier, J -- deBuizer, J -- Dekany, R -- de Leon, J -- Dello Russo, N -- Delsanti, A -- DiSanti, M -- Drummond, J -- Dundon, L -- Etzel, P B -- Farnham, T L -- Feldman, P -- Fernandez, Y R -- Filipovic, M D -- Fisher, S -- Fitzsimmons, A -- Fong, D -- Fugate, R -- Fujiwara, H -- Fujiyoshi, T -- Furusho, R -- Fuse, T -- Gibb, E -- Groussin, O -- Gulkis, S -- Gurwell, M -- Hadamcik, E -- Hainaut, O -- Harker, D -- Harrington, D -- Harwit, M -- Hasegawa, S -- Hergenrother, C W -- Hirst, P -- Hodapp, K -- Honda, M -- Howell, E S -- Hutsemekers, D -- Iono, D -- Ip, W-H -- Jackson, W -- Jehin, E -- Jiang, Z J -- Jones, G H -- Jones, P A -- Kadono, T -- Kamath, U W -- Kaufl, H U -- Kasuga, T -- Kawakita, H -- Kelley, M S -- Kerber, F -- Kidger, M -- Kinoshita, D -- Knight, M -- Lara, L -- Larson, S M -- Lederer, S -- Lee, C-F -- Levasseur-Regourd, A C -- Li, J Y -- Li, Q-S -- Licandro, J -- Lin, Z-Y -- Lisse, C M -- LoCurto, G -- Lovell, A J -- Lowry, S C -- Lyke, J -- Lynch, D -- Ma, J -- Magee-Sauer, K -- Maheswar, G -- Manfroid, J -- Marco, O -- Martin, P -- Melnick, G -- Miller, S -- Miyata, T -- Moriarty-Schieven, G H -- Moskovitz, N -- Mueller, B E A -- Mumma, M J -- Muneer, S -- Neufeld, D A -- Ootsubo, T -- Osip, D -- Pandea, S K -- Pantin, E -- Paterno-Mahler, R -- Patten, B -- Penprase, B E -- Peck, A -- Petitas, G -- Pinilla-Alonso, N -- Pittichova, J -- Pompei, E -- Prabhu, T P -- Qi, C -- Rao, R -- Rauer, H -- Reitsema, H -- Rodgers, S D -- Rodriguez, P -- Ruane, R -- Ruch, G -- Rujopakarn, W -- Sahu, D K -- Sako, S -- Sakon, I -- Samarasinha, N -- Sarkissian, J M -- Saviane, I -- Schirmer, M -- Schultz, P -- Schulz, R -- Seitzer, P -- Sekiguchi, T -- Selman, F -- Serra-Ricart, M -- Sharp, R -- Snell, R L -- Snodgrass, C -- Stallard, T -- Stecklein, G -- Sterken, C -- Stuwe, J A -- Sugita, S -- Sumner, M -- Suntzeff, N -- Swaters, R -- Takakuwa, S -- Takato, N -- Thomas-Osip, J -- Thompson, E -- Tokunaga, A T -- Tozzi, G P -- Tran, H -- Troy, M -- Trujillo, C -- Van Cleve, J -- Vasundhara, R -- Vazquez, R -- Vilas, F -- Villanueva, G -- von Braun, K -- Vora, P -- Wainscoat, R J -- Walsh, K -- Watanabe, J -- Weaver, H A -- Weaver, W -- Weiler, M -- Weissman, P R -- Welsh, W F -- Wilner, D -- Wolk, S -- Womack, M -- Wooden, D -- Woodney, L M -- Woodward, C -- Wu, Z-Y -- Wu, J-H -- Yamashita, T -- Yang, B -- Yang, Y-B -- Yokogawa, S -- Zook, A C -- Zauderer, A -- Zhao, X -- Zhou, X -- Zucconi, J-M -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):265-9. Epub 2005 Sep 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Astronomy, University of Hawaii at Manoa, 2680 Woodlawn Drive, Honolulu, HI 96822, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16150977" target="_blank"〉PubMed〈/a〉
    Keywords: Cosmic Dust ; Jupiter ; *Meteoroids ; Organic Chemicals ; Photometry
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2005-09-17
    Description: The impact cratering process on a comet is controversial but holds the key for interpreting observations of the Deep Impact collision with comet 9P/Tempel 1. Mid-infrared data from the Cooled Mid-Infrared Camera and Spectrometer (COMICS) of the Subaru Telescope indicate that the large-scale dust plume ejected by the impact contained a large mass (approximately 10(6) kilograms) of dust and formed two wings approximately +/-45 degrees from the symmetric center, both consistent with gravity as the primary control on the impact and its immediate aftermath. The dust distribution in the inner part of the plume, however, is inconsistent with a pure gravity control and implies that evaporation and expansion of volatiles accelerated dust.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sugita, S -- Ootsubo, T -- Kadono, T -- Honda, M -- Sako, S -- Miyata, T -- Sakon, I -- Yamashita, T -- Kawakita, H -- Fujiwara, H -- Fujiyoshi, T -- Takato, N -- Fuse, T -- Watanabe, J -- Furusho, R -- Hasegawa, S -- Kasuga, T -- Sekiguchi, T -- Kinoshita, D -- Meech, K J -- Wooden, D H -- Ip, W H -- A'Hearn, M F -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):274-8. Epub 2005 Sep 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Complexity Science and Engineering, University of Tokyo, Kashiwa, Chiba, Japan. sugita@k.u-tokyo.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16166476" target="_blank"〉PubMed〈/a〉
    Keywords: Cosmic Dust ; Jupiter ; *Meteoroids ; Spectrophotometry, Infrared ; Volatilization
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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