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01000naa a22002652 4500 |
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NLM142415162 |
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DE-627 |
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20231223024511.0 |
| 007 |
tu |
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231223s2003 xx ||||| 00| ||eng c |
| 028 |
5 |
2 |
|a pubmed24n0475.xml
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| 035 |
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|a (DE-627)NLM142415162
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| 035 |
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|a (NLM)14499241
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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 Kim, Kyoung Soo
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a In vitro and in vivo T cell oligoclonality following chronic stimulation with staphylococcal superantigens
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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 30.10.2003
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| 500 |
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|a Date Revised 08.11.2019
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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 Microbial superantigens (SAg), including SEB and TSST-1, polyclonally activate T cells belonging to specific TCR BV families. A pathogenic role for SAg in various human diseases has been suggested, but enthusiasm for this view has been tempered by the T cell oligoclonality in these disorders. To assess whether T cell oligoclonality can emerge following protracted SAg stimulation, human PBMC were stimulated with SEB, TSST-1, or anti-CD3 mAb and maintained in culture with exogenous IL-2. Oligoclonality was appreciated by day 14 among CD4(+) and CD8(+) T cells. In addition, mice transgenic for human DR2 and DQ8 were injected weekly with SEB, and splenic CD4(+) and CD8(+) T cells were analyzed for oligoclonality. In mice that received one or three such injections, little-to-no oligoclonality was detected. In contrast, considerable oligoclonality was detected in mice that received eight weekly SEB injections. Many of these T cell oligoclones were identical to "spontaneously" arising oligoclones detected in SEB-naive mice. Thus, T cell oligoclonality can emerge following chronic SAg stimulation. In hosts who have lost tolerance to self Ag, chronic exposure to SAg may preferentially promote expansion of autoreactive T cells and facilitate development of clinical disease
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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 Bacterial Toxins
|2 NLM
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| 650 |
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7 |
|a Complementarity Determining Regions
|2 NLM
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| 650 |
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7 |
|a Enterotoxins
|2 NLM
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| 650 |
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7 |
|a HLA-DQ Antigens
|2 NLM
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| 650 |
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7 |
|a HLA-DQ8 antigen
|2 NLM
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| 650 |
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7 |
|a HLA-DR2 Antigen
|2 NLM
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| 650 |
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7 |
|a Superantigens
|2 NLM
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| 650 |
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7 |
|a enterotoxin F, Staphylococcal
|2 NLM
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| 650 |
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7 |
|a enterotoxin B, staphylococcal
|2 NLM
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| 650 |
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7 |
|a 39424-53-8
|2 NLM
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| 700 |
1 |
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|a Jacob, Noam
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Stohl, William
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 108(2003), 3 vom: 19. Sept., Seite 182-9
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:108
|g year:2003
|g number:3
|g day:19
|g month:09
|g pages:182-9
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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 108
|j 2003
|e 3
|b 19
|c 09
|h 182-9
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