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20250217222338.0 |
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231224s2015 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2014.12.002
|2 doi
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|a pubmed25n0815.xml
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|a (DE-627)NLM244630771
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|a (NLM)25513733
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|a (PII)S1521-6616(14)00269-1
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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 Fousteri, Georgia
|e verfasserin
|4 aut
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1 |
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|a PTPN22 controls virally-induced autoimmune diabetes by modulating cytotoxic T lymphocyte responses in an epitope-specific manner
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|c 2015
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 30.04.2015
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|a Date Revised 20.02.2015
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2014 Elsevier Inc. All rights reserved.
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|a Ptpn22 is one of the most potent autoimmunity predisposing genes and strongly associates with type 1 diabetes (T1D). Previous studies showed that non-obese diabetic mice with reduced expression levels of Ptpn22 are protected from T1D due to increased number of T regulatory (Treg) cells. We report that lack of Ptpn22 exacerbates virally-induced T1D in female rat insulin promoter lymphocytic choriomeningitis virus (RIP-LCMV-GP) mice, while maintaining higher number of Treg cells throughout the antiviral response in the blood and spleen but not in the pancreatic lymph nodes. GP33-41-specific pentamer-positive cytotoxic lymphocytes (CTLs) are numerically reduced in the absence of Ptpn22 at the expansion and contraction phase but reach wild-type levels at the memory phase. However, they show similar effector function and even a subtle increase in the production of IL-2. In contrast, NP396-404-specific CTLs develop normally at all phases but display enhanced effector function. Lack of Ptpn22 also augments the memory proinflammatory response of GP61-80 CD4 T cells. Hence, lack of Ptpn22 largely augments antiviral effector T cell responses, suggesting that caution should be taken when targeting Ptpn22 to treat autoimmune diseases where viral infections are considered environmental triggers
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| 650 |
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4 |
|a Journal Article
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4 |
|a Research Support, Non-U.S. Gov't
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4 |
|a Cytotoxic lymphocytes (CTLs);
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| 650 |
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4 |
|a Memory CD8(+) T cells;
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| 650 |
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4 |
|a Ptpn22;
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| 650 |
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|a Treg cells
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| 650 |
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4 |
|a Type 1 diabetes (T1D);
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| 650 |
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4 |
|a Virally-induced T1D;
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| 650 |
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7 |
|a Epitopes, T-Lymphocyte
|2 NLM
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| 650 |
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7 |
|a Protein Tyrosine Phosphatase, Non-Receptor Type 22
|2 NLM
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| 650 |
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7 |
|a EC 3.1.3.48
|2 NLM
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| 650 |
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7 |
|a Ptpn22 protein, mouse
|2 NLM
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| 650 |
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7 |
|a EC 3.1.3.48
|2 NLM
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| 700 |
1 |
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|a Jofra, Tatiana
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Di Fonte, Roberta
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Kuka, Mirela
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Iannacone, Matteo
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Battaglia, Manuela
|e verfasserin
|4 aut
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| 773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 156(2015), 2 vom: 02. Feb., Seite 98-108
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:156
|g year:2015
|g number:2
|g day:02
|g month:02
|g pages:98-108
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2014.12.002
|3 Volltext
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|a GBV_ILN_11
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|d 156
|j 2015
|e 2
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|h 98-108
|