# |
PMID |
Sentence |
1 |
19797268
|
Upon Leishmania-macrophage interaction, activation of the protein tyrosine phosphatase (PTP) SHP-1 rapidly leads to the down-regulation of Janus kinase and mitogen-activated protein kinase signaling, resulting in the attenuation of host innate inflammatory responses and of various microbicidal macrophage functions.
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2 |
19797268
|
We report that, in addition to SHP-1, the PTPs PTP1B and TCPTP are activated and posttranslationally modified in infected macrophages, and we identify an essential role for PTP1B in the in vivo progression of Leishmania infection.
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3 |
19797268
|
Access of GP63 to macrophage PTP1B, TCPTP, and SHP-1 is mediated in part by a lipid raft-dependent mechanism, resulting in PTP cleavage and stimulation of phosphatase activity.
|
4 |
19797268
|
Upon Leishmania-macrophage interaction, activation of the protein tyrosine phosphatase (PTP) SHP-1 rapidly leads to the down-regulation of Janus kinase and mitogen-activated protein kinase signaling, resulting in the attenuation of host innate inflammatory responses and of various microbicidal macrophage functions.
|
5 |
19797268
|
We report that, in addition to SHP-1, the PTPs PTP1B and TCPTP are activated and posttranslationally modified in infected macrophages, and we identify an essential role for PTP1B in the in vivo progression of Leishmania infection.
|
6 |
19797268
|
Access of GP63 to macrophage PTP1B, TCPTP, and SHP-1 is mediated in part by a lipid raft-dependent mechanism, resulting in PTP cleavage and stimulation of phosphatase activity.
|
7 |
24997008
|
The protein tyrosine phosphatase N2 (PTPN2) attenuates T cell receptor (TCR) signalling and tunes CD8(+) T cell responses in vivo.
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8 |
24997008
|
The transfer of OVA-specific OT-I CD8(+) T cells (C57BL/6) into RIP-mOVA recipients expressing OVA in pancreatic β-cells only results in islet destruction when OVA-specific CD4(+) T cells are co-transferred.
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9 |
24997008
|
Herein we report that PTPN2-deficient OT-I CD8(+) T cells transferred into RIP-mOVA recipients acquire CTL activity and result in β cell destruction and the development of diabetes in the absence of CD4(+) help.
|
10 |
24997008
|
These studies identify PTPN2 as a critical mediator of peripheral T cell tolerance limiting CD8(+) T cell responses after the cross-presentation of self-antigens.
|
11 |
24997008
|
Our findings reveal a mechanism by which PTPN2 SNPs might convert a tolerogenic CD8(+) T cell response into one capable of causing the destruction of pancreatic β-cells.
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12 |
24997008
|
The protein tyrosine phosphatase N2 (PTPN2) attenuates T cell receptor (TCR) signalling and tunes CD8(+) T cell responses in vivo.
|
13 |
24997008
|
The transfer of OVA-specific OT-I CD8(+) T cells (C57BL/6) into RIP-mOVA recipients expressing OVA in pancreatic β-cells only results in islet destruction when OVA-specific CD4(+) T cells are co-transferred.
|
14 |
24997008
|
Herein we report that PTPN2-deficient OT-I CD8(+) T cells transferred into RIP-mOVA recipients acquire CTL activity and result in β cell destruction and the development of diabetes in the absence of CD4(+) help.
|
15 |
24997008
|
These studies identify PTPN2 as a critical mediator of peripheral T cell tolerance limiting CD8(+) T cell responses after the cross-presentation of self-antigens.
|
16 |
24997008
|
Our findings reveal a mechanism by which PTPN2 SNPs might convert a tolerogenic CD8(+) T cell response into one capable of causing the destruction of pancreatic β-cells.
|
17 |
24997008
|
The protein tyrosine phosphatase N2 (PTPN2) attenuates T cell receptor (TCR) signalling and tunes CD8(+) T cell responses in vivo.
|
18 |
24997008
|
The transfer of OVA-specific OT-I CD8(+) T cells (C57BL/6) into RIP-mOVA recipients expressing OVA in pancreatic β-cells only results in islet destruction when OVA-specific CD4(+) T cells are co-transferred.
|
19 |
24997008
|
Herein we report that PTPN2-deficient OT-I CD8(+) T cells transferred into RIP-mOVA recipients acquire CTL activity and result in β cell destruction and the development of diabetes in the absence of CD4(+) help.
|
20 |
24997008
|
These studies identify PTPN2 as a critical mediator of peripheral T cell tolerance limiting CD8(+) T cell responses after the cross-presentation of self-antigens.
|
21 |
24997008
|
Our findings reveal a mechanism by which PTPN2 SNPs might convert a tolerogenic CD8(+) T cell response into one capable of causing the destruction of pancreatic β-cells.
|
22 |
24997008
|
The protein tyrosine phosphatase N2 (PTPN2) attenuates T cell receptor (TCR) signalling and tunes CD8(+) T cell responses in vivo.
|
23 |
24997008
|
The transfer of OVA-specific OT-I CD8(+) T cells (C57BL/6) into RIP-mOVA recipients expressing OVA in pancreatic β-cells only results in islet destruction when OVA-specific CD4(+) T cells are co-transferred.
|
24 |
24997008
|
Herein we report that PTPN2-deficient OT-I CD8(+) T cells transferred into RIP-mOVA recipients acquire CTL activity and result in β cell destruction and the development of diabetes in the absence of CD4(+) help.
|
25 |
24997008
|
These studies identify PTPN2 as a critical mediator of peripheral T cell tolerance limiting CD8(+) T cell responses after the cross-presentation of self-antigens.
|
26 |
24997008
|
Our findings reveal a mechanism by which PTPN2 SNPs might convert a tolerogenic CD8(+) T cell response into one capable of causing the destruction of pancreatic β-cells.
|