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01000naa a22002652 4500 |
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NLM108858502 |
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DE-627 |
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20231222150109.0 |
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231222s2000 xx ||||| 00| ||eng c |
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|a pubmed24n0363.xml
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|a (DE-627)NLM108858502
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|a (NLM)10964538
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Xu, L Y
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a Combined nasal administration of encephalitogenic myelin basic protein peptide 68-86 and IL-10 suppressed incipient experimental allergic encephalomyelitis in Lewis rats
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| 264 |
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1 |
|c 2000
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| 336 |
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|a Text
|b txt
|2 rdacontent
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| 337 |
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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 22.09.2000
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| 500 |
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|a Date Revised 30.11.2018
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| 500 |
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|a published: Print
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| 500 |
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|a Citation Status MEDLINE
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| 520 |
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|a Copyright 2000 Academic Press.
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| 520 |
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|a Mucosal administration of low doses of myelin basic protein (MBP) peptide 68-86 (MBP 68-86) or anti-inflammatory cytokine IL-10 effectively prevented experimental allergic encephalomyelitis (EAE), but failed to suppress the disease if given after 7 days postimmunization (p.i.), i.e., after T cell priming had occurred. We anticipated that combined administration of autoantigen and IL-10 can treat incipient EAE. Lewis rats with EAE actively induced with MBP 68-86 and complete Freund's adjuvant received 120 microg MBP 68-86 + 200 ng IL-10 per rat per day from day 7 p.i. and for 5 consecutive days. These rats showed later onset, lower clinical scores, less body weight loss, and shorter duration of EAE than rats receiving MBP 68-86 or IL-10 only or PBS. EAE amelioration was associated with decreased infiltration of ED1(+) macrophages and CD4(+) T cells within the central nervous system and with decreased proliferative responses of lymph node cells, indicating that combined administration of MBP 68-86 and IL-10 induced immune hyporesponsiveness. IFN-gamma secretion as well as IFN-gamma, TNF-alpha, IL-4, and IL-10 mRNA expression by lymph node MNC was down-regulated in the treated rats. Immune hyporesponsiveness, rather than immune deviation or regulatory mechanisms, seems to be responsible for the protection of EAE after autoantigen + IL-10 administration by the nasal route
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| 650 |
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4 |
|a Journal Article
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| 650 |
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4 |
|a Research Support, Non-U.S. Gov't
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| 650 |
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7 |
|a Antigens
|2 NLM
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| 650 |
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7 |
|a Cytokines
|2 NLM
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| 650 |
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7 |
|a Myelin Basic Protein
|2 NLM
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| 650 |
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7 |
|a Peptide Fragments
|2 NLM
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| 650 |
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7 |
|a RNA, Messenger
|2 NLM
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| 650 |
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7 |
|a myelin basic protein 68-86
|2 NLM
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| 650 |
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7 |
|a Interleukin-10
|2 NLM
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| 650 |
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7 |
|a 130068-27-8
|2 NLM
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| 650 |
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7 |
|a Interferon-gamma
|2 NLM
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| 650 |
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7 |
|a 82115-62-6
|2 NLM
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| 700 |
1 |
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|a Yang, J S
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Huang, Y M
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Levi, M
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Link, H
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Xiao, B G
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 96(2000), 3 vom: 01. Sept., Seite 205-11
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:96
|g year:2000
|g number:3
|g day:01
|g month:09
|g pages:205-11
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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 96
|j 2000
|e 3
|b 01
|c 09
|h 205-11
|