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01000naa a22002652 4500 |
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NLM142415200 |
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DE-627 |
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20231223024511.0 |
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tu |
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231223s2003 xx ||||| 00| ||eng c |
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|a pubmed24n0475.xml
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|a (DE-627)NLM142415200
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| 035 |
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|a (NLM)14499245
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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 Wei, Yongzhong
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a FLIP and FasL expression by inflammatory cells vs thyrocytes can be predictive of chronic inflammation or resolution of autoimmune thyroiditis
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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 Spontaneous autoimmune thyroiditis (SAT) in NOD.H-2h4 mice is a model of chronic inflammation of the thyroid, while granulomatous experimental autoimmune thyroiditis (G-EAT) is a model with spontaneous resolution of inflammation. In chronic inflammation (SAT), Fas, FasL, and FLIP were upregulated and predominant in inflammatory cells. There were few apoptotic cells, and low expression of active caspase-8 and -3. In resolving G-EAT in CBA/J and NOD.H-2h4 mice, FasL and FLIP were predominantly expressed by thyrocytes. There were many apoptotic inflammatory cells, and increased expression of active caspase-8 and -3. Depletion of CD8+ T cells inhibited G-EAT resolution and resulted in chronic inflammation. FLIP was expressed predominantly by inflammatory cells, and apoptosis of inflammatory cells and expression of active caspase-3 was reduced as in chronic SAT. Thus, differences in expression of pro- or antiapoptotic molecules in SAT or G-EAT were apparently related to the acute vs chronic nature of the inflammatory response rather than the method of disease induction. Upregulation of FLIP by inflammatory cells may block Fas-mediated apoptosis, contributing to chronic inflammation, whereas increased FLIP expression by thyrocytes in resolving G-EAT may protect thyrocytes from apoptosis, and FasL expression by thyrocytes may induce apoptosis of inflammatory cells, contributing to resolution
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| 650 |
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4 |
|a Comparative Study
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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 CASP8 and FADD-Like Apoptosis Regulating Protein
|2 NLM
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| 650 |
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7 |
|a Carrier Proteins
|2 NLM
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| 650 |
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7 |
|a Cflar protein, mouse
|2 NLM
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| 650 |
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7 |
|a Fas Ligand Protein
|2 NLM
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| 650 |
|
7 |
|a Fasl protein, mouse
|2 NLM
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| 650 |
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7 |
|a Intracellular Signaling Peptides and Proteins
|2 NLM
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| 650 |
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7 |
|a Membrane Glycoproteins
|2 NLM
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| 650 |
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7 |
|a Casp3 protein, mouse
|2 NLM
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| 650 |
|
7 |
|a EC 3.4.22.-
|2 NLM
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| 650 |
|
7 |
|a Casp8 protein, mouse
|2 NLM
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| 650 |
|
7 |
|a EC 3.4.22.-
|2 NLM
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| 650 |
|
7 |
|a Casp9 protein, mouse
|2 NLM
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| 650 |
|
7 |
|a EC 3.4.22.-
|2 NLM
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| 650 |
|
7 |
|a Caspase 3
|2 NLM
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| 650 |
|
7 |
|a EC 3.4.22.-
|2 NLM
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| 650 |
|
7 |
|a Caspase 8
|2 NLM
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| 650 |
|
7 |
|a EC 3.4.22.-
|2 NLM
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| 650 |
|
7 |
|a Caspase 9
|2 NLM
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| 650 |
|
7 |
|a EC 3.4.22.-
|2 NLM
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| 650 |
|
7 |
|a Caspases
|2 NLM
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| 650 |
|
7 |
|a EC 3.4.22.-
|2 NLM
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| 700 |
1 |
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|a Chen, Kemin
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Sharp, Gordon C
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Braley-Mullen, Helen
|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 221-33
|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:221-33
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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
|
| 912 |
|
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|a GBV_ILN_24
|
| 912 |
|
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|a GBV_ILN_350
|
| 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 221-33
|