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231222s2001 xx ||||| 00| ||eng c |
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|a pubmed24n0369.xml
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|a (DE-627)NLM11055261X
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|a (NLM)11141334
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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 Miyaguchi, S
|e verfasserin
|4 aut
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|a Human LT-alpha-mediated resistance to autoimmune diabetes is induced in NOD, but not NOD-scid, mice and abrogated by IL-12
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|c 2001
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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 22.02.2001
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|a Date Revised 21.11.2008
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|a published: Print
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|a Citation Status MEDLINE
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| 520 |
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|a Copyright 2001 Academic Press.
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|a Systemic administration of human lymphotoxin-alpha (hLT-alpha) made NOD mice resistant not only to spontaneous autoimmune type 1 diabetes mellitus but also to cyclophosphamide (CY)-induced diabetes and diabetes transfer by diabetic NOD spleen cells (triple resistance). In this study we analyzed the mechanisms of hLT-alpha-induced resistance, focusing on (1) hLT-alpha-induced resistance in the pancreatic beta cell, (2) CY-resistant suppressor cells, (3) suppression of induction or function of effector cells for beta cell destruction, or (4) others. To examine the first possibility in vitro, a NOD-derived beta cell line (MIN6N) was pretreated with hLT-alpha and then mixed with diabetic NOD spleen cells and MIN6N cell viability was measured. Treatment with hLT-alpha did not protect MIN6N cells but rather enhanced cytotoxicity. Next NOD-scid mice were pretreated with hLT-alpha and then transferred with diabetic NOD spleen. All the recipients developed diabetes. These results excluded the first possibility. The second possibility was also excluded by a cotransfer experiment, in which diabetic NOD spleen cells were cotransferred to NOD-scid mice with nontreated or hLT-alpha-treated nondiabetic NOD spleens. There was no significant difference in diabetes incidence between the two groups. To observe the third possibility, spleen cells of hLT-alpha-treated triple-resistant NOD mice were transferred to NOD-scid mice. Diabetes developed in the recipients, although the onset of diabetes was slightly delayed. Finally, hLT-alpha-treated triple-resistant NOD mice developed diabetes 1 week after daily IL-12 treatment. In summary, hLT-alpha administration made NOD mice resistant to effector cells for beta cell destruction. This resistance was induced in NOD, but not in NOD-scid, mice, indicating that lymphocytes were obligatory for the resistance. However, it was not mediated by transferable suppressor cells. Because effector cells were present in hLT-alpha-treated NOD spleen and the resistance was abrogated by IL-12 treatment, it is speculated that hLT-alpha treatment may have changed a local cytokine balance protective from beta cell destruction
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| 650 |
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|a Journal Article
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| 650 |
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|a Lymphotoxin-alpha
|2 NLM
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| 650 |
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|a Interleukin-12
|2 NLM
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| 650 |
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|a 187348-17-0
|2 NLM
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| 700 |
1 |
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|a Satoh, J
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Takahashi, K
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Sakata, Y
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Nakazawa, T
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Miyazaki, J
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Toyota, T
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 98(2001), 1 vom: 01. Jan., Seite 119-24
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:98
|g year:2001
|g number:1
|g day:01
|g month:01
|g pages:119-24
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| 912 |
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|a GBV_USEFLAG_A
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| 912 |
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|a SYSFLAG_A
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| 912 |
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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 98
|j 2001
|e 1
|b 01
|c 01
|h 119-24
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