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01000naa a22002652 4500 |
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NLM124775330 |
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DE-627 |
| 005 |
20231222204300.0 |
| 007 |
tu |
| 008 |
231222s2003 xx ||||| 00| ||eng c |
| 028 |
5 |
2 |
|a pubmed24n0416.xml
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| 035 |
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|a (DE-627)NLM124775330
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| 035 |
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|a (NLM)12706402
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| 040 |
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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 Schmied, M
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a In vitro evidence that subcutaneous administration of glatiramer acetate induces hyporesponsive T cells in patients with multiple sclerosis
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| 264 |
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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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| 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 15.05.2003
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| 500 |
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|a Date Revised 07.11.2019
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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 Glatiramer acetate (GA; Copaxone) is a random sequence polypeptide used in the treatment of relapsing remitting multiple sclerosis (RR MS). We have recently demonstrated that prior to treatment, GA induces proliferation of resting T cells and is not cross-reactive with myelin antigens. Daily GA injections induce a significant loss of this GA responsiveness, which is associated with the induction of highly cross-reactive Th2-type T cells potentially capable of suppressing inflammatory responses. The mechanism of action by which GA induces T cell nonresponsiveness leading to T cell receptor degeneracy in patients with RR MS is unknown. Here, we examined the effects of daily GA administration on the induction of T cell hyporesponsiveness. The frequency of GA-reactive T cells in peripheral blood of seven patients with RR MS was measured by limiting dilution analysis prior to and during 6 months of treatment. In addition, a model in which GA-reactive T cells were stimulated in vitro was developed to better characterize the selection of T cell populations over time. In vivo treatment with GA induced a decrease in GA-reactive T cell frequencies and hyporesponsiveness of CD4(+) T cell reactivity to GA in vitro that was only partially reversed by the addition of IL-2. These data suggest that T cell peripheral tolerance to GA was achieved in vivo during treatment. Thus, our in vitro data suggest that the underlying changes in GA-reactive CD4(+) T cell reactivity could be explained by the induction of T cell anergy and clonal elimination
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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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4 |
|a Research Support, U.S. Gov't, P.H.S.
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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 Interleukin-2
|2 NLM
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| 650 |
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7 |
|a Peptides
|2 NLM
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| 650 |
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7 |
|a Recombinant Proteins
|2 NLM
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| 650 |
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7 |
|a Glatiramer Acetate
|2 NLM
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| 650 |
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7 |
|a 5M691HL4BO
|2 NLM
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| 700 |
1 |
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|a Duda, P W
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Krieger, J I
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Trollmo, C
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Hafler, D A
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 106(2003), 3 vom: 01. März, Seite 163-74
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:106
|g year:2003
|g number:3
|g day:01
|g month:03
|g pages:163-74
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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 106
|j 2003
|e 3
|b 01
|c 03
|h 163-74
|