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NLM143160281 |
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DE-627 |
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231223s2003 xx ||||| 00| ||eng c |
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|a pubmed24n0477.xml
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|a (DE-627)NLM143160281
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|a (NLM)14597220
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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100 |
1 |
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|a Watanabe, Shiro
|e verfasserin
|4 aut
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245 |
1 |
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|a Kinetic analysis of the development of pancreatic lesions in mice infected with a murine retrovirus
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1 |
|c 2003
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336 |
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|a Text
|b txt
|2 rdacontent
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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338 |
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|a Band
|b nc
|2 rdacarrier
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500 |
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|a Date Completed 11.12.2003
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|a Date Revised 08.11.2019
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|a published: Print
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|a Citation Status MEDLINE
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|a Sjögren's syndrome (SjS)-like sialoadenitis and exocrine pancreatitis were induced in mice infected with LP-BM5 murine leukemia virus, which induces a severe immunodeficiency termed murine AIDS (MAIDS). All mice with MAIDS showed advancing cellular infiltration around the pancreatic ducts as well as systemic exocrinopathy. The primary target tissue of the pancreas was acinar cells, and the pancreatic islets were well preserved until a late phase of the disease. Immunofluorescence and flow cytometry demonstrated that CD4(+) T cells, Mac-1(+) cells, and B220(+) cells were major inflammatory components, and IFN-gamma and IL-10 were mainly detected on CD4(+) T and Mac-1(+) cells in the pancreas. Both Th1 and Th2 cells were found. TUNEL(+) apoptotic cells were mostly detected among pancreas-infiltrating cells. Fas ligand and TNF-alpha were also detected among pancreas-infiltrating cells, whereas Fas was rarely expressed in the pancreatic acinar cells. Thus, MAIDS mice could be valuable for analyzing the pathogenesis of autoimmune-related pancreatitis associated with SjS
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|a Journal Article
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650 |
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|a Research Support, Non-U.S. Gov't
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650 |
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7 |
|a Cytokines
|2 NLM
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|a DNA, Viral
|2 NLM
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650 |
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7 |
|a RNA
|2 NLM
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650 |
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7 |
|a 63231-63-0
|2 NLM
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700 |
1 |
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|a Suzuki, Kenji
|e verfasserin
|4 aut
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700 |
1 |
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|a Kawauchi, Yusuke
|e verfasserin
|4 aut
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700 |
1 |
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|a Yamagiwa, Satoshi
|e verfasserin
|4 aut
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700 |
1 |
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|a Yoneyama, Hiroyuki
|e verfasserin
|4 aut
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700 |
1 |
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|a Kawachi, Hiroshi
|e verfasserin
|4 aut
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700 |
1 |
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|a Okada, Yoshiaki
|e verfasserin
|4 aut
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700 |
1 |
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|a Shimizu, Fujio
|e verfasserin
|4 aut
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700 |
1 |
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|a Asakura, Hitoshi
|e verfasserin
|4 aut
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700 |
1 |
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|a Aoyagi, Yutaka
|e verfasserin
|4 aut
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773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 109(2003), 2 vom: 15. Nov., Seite 212-23
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
|
773 |
1 |
8 |
|g volume:109
|g year:2003
|g number:2
|g day:15
|g month:11
|g pages:212-23
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912 |
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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912 |
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|a GBV_ILN_11
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912 |
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|a GBV_ILN_24
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912 |
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|a GBV_ILN_350
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951 |
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|a AR
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952 |
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|d 109
|j 2003
|e 2
|b 15
|c 11
|h 212-23
|