Non-conventional signal transduction by type 1 interferons: The NF-κB pathway

2007 ◽  
Vol 102 (5) ◽  
pp. 1087-1094 ◽  
Author(s):  
Ziyun Du ◽  
Lai Wei ◽  
Aruna Murti ◽  
Susan R. Pfeffer ◽  
Meiyun Fan ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Conventional Signal ◽  
Type 1 Interferons

Lipid signal transduction pathways in angiotensin II type 1 receptor-transfected fibroblasts

1995 ◽  
Vol 269 (2) ◽  
pp. C435-C442 ◽  
Author(s):  
Y. Wen ◽  
M. C. Cabot ◽  
E. Clauser ◽  
S. L. Bursten ◽  
J. L. Nadler
Keyword(s):  
Signal Transduction ◽  
Angiotensin Ii ◽  
Chinese Hamster ◽  
Receptor Activation ◽  
Signal Transduction Pathways ◽  
Ang Ii ◽  
Vascular Type ◽  
Lipid Signal ◽  
Fibroblast Line

A stable Chinese hamster ovary fibroblast line expressing the rat vascular type 1a angiotensin II (ANG II) receptor was used to study the lipid-derived signal transduction pathways elicited by type 1a ANG II receptor activation. ANG II caused a biphasic and dose-dependent increase in diacylglycerol (DAG) accumulation with an initial peak at 15 s (181 +/- 11% of control, P < 0.02) and a second sustained peak at 5-10 min (214 +/- 10% of control, P < 0.02). The late DAG peak was derived from phosphatidylcholine (PC), and the formation was blocked by ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. ANG II also increased phosphatidic acid (PA) production nearly fourfold by 7.5 min. In the presence of ethanol, ANG II markedly increased phosphatidylethanol (PEt) formation, indicating activation of phospholipase D (PLD). ANG II was shown to increase the mass of three separate PA species, one of which apparently originated from DAG kinase action on PC-phospholipase C (PLC)-produced DAG, providing evidence for PC-PLC activity. ANG II also formed a third PA species, which originated neither from PLD nor from DAG kinase. These results demonstrate that multiple lipid signals propagated via collateral stimulation of PLC and PLD are generated by specific activation of the vascular type 1a ANG II receptor.

scholarly journals Type 1 Interferons Suppress Accelerated Osteoclastogenesis and Prevent Loss of Bone Mass During Systemic Inflammatory Responses to Pneumocystis Lung Infection

2012 ◽  
Vol 181 (1) ◽  
pp. 151-162 ◽  
Author(s):  
Michelle Wilkison ◽  
Katherine Gauss ◽  
Yanchao Ran ◽  
Steve Searles ◽  
David Taylor ◽  
...  
Keyword(s):  
Bone Mass ◽  
Inflammatory Responses ◽  
Lung Infection ◽  
Type 1 Interferons

A rapid and efficient method for generating anti-variable region monoclonal antibodies using type-1 interferons as immune modulators

2006 ◽  
Vol 15 (3) ◽  
pp. 61-69 ◽  
Author(s):  
Kimberly Staquet ◽  
Jamie Fisher ◽  
Roberta Lamb ◽  
Gregory Bannish ◽  
Cynthia Duchala ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Efficient Method ◽  
Variable Region ◽  
Immune Modulators ◽  
Type 1 Interferons

scholarly journals The role of type 1 interferons in Gram-negative bacteria-induced coagulation

Blood ◽  
2020 ◽  
Author(s):  
Xinyu Yang ◽  
Xiaoye Cheng ◽  
Yiting Tang ◽  
Xianhui Qiu ◽  
Zhongtai Wang ◽  
...  
Keyword(s):  
Immune Responses ◽  
Bacterial Infection ◽  
Innate Immune ◽  
Coagulation Cascade ◽  
Outer Cell ◽  
Gram Negative Bacteria ◽  
Innate Immune Responses ◽  
Gram Negative ◽  
Type 1 Interferons

Bacterial infection not only stimulates innate immune responses but also activates the coagulation cascades. Over-activation of the coagulation system in bacterial sepsis leads to disseminated intravascular coagulation (DIC), a life-threatening condition. However, the mechanisms by which bacterial infection activates the coagulation cascade are not fully understood. Here we show that type 1 interferons (IFNs), widely expressed family of cytokines that orchestrate innate antiviral and antibacterial immunity, mediate bacterial infection-induced DIC through amplifying the release of high mobility box group box 1 (HMGB1) into the blood stream. Inhibition of the expression of type 1 IFNs, disruption of their receptor IFN-α/βR or downstream effector (e.g., HMGB1) uniformly decreased Gram-negative bacteria-induced DIC. Mechanistically, extracellular HMGB1 markedly increased the pro-coagulant activity of tissue factor (TF) by promoting the externalization of phosphatidylserine (PS) to the outer cell surface, where PS assembles a complex of cofactor-proteases of the coagulation cascades. These findings not only provide novel insights into the link between innate immune responses and coagulation, but also open a new avenue for developing novel therapeutic strategies to prevent DIC in sepsis.

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