scholarly journals PD-1 /PD-L1 Adoptive Checkpoint Biosynthesis Separately Are Regulated By Gamma Common Which Regulate PD-1, Globin, and IFN-Gamma

2021 ◽  
pp. 1-9
Author(s):  
Ashraf Marzouk El Tantawi ◽  
Keyword(s):  
T Cells ◽  
Tyrosine Kinases ◽  
Adaptor Protein ◽  
Cytokine Signaling ◽  
Immune Functions ◽  
Suppressor Of Cytokine Signaling ◽  
Ifn Gamma ◽  
Helical Proteins

PD-1 /PD-L1 is adoptive checkpoint mechanism, where PD-1 is an adopting its PD-L1 ligand activities by presence of specific helical kinase proteins in its compositions: _gamma common chains,_LNK” lymphocyte adaptor protein, _or SH2B adaptor _protein “tyrosine kinases, and _”SOCS” suppressor of cytokine signaling, that specified for controlling PD-1 and PD-L1 bindings activity through temporary resting the PD-L1 and consequently T-cells activities then transform incoming signals to exogenous processes in favor the of proper immune functions, But the permanent inhibition of PD-1 /PD-L1 binding is due to breaking down or inhibition in one or more of the adaptors helical proteins (lymphocyte adaptor protein, or SH2B) with the presence of SOCS” suppressor of cytokine signaling that will increase stability of binding without adopting and without activities, but cells survival can still exist through presence of tyrosine kinases , interferon stimulate kinases ,and gamma common.

scholarly journals Forced expression of suppressor of cytokine signaling 3 in T cells protects the development of concanavalin A-induced hepatitis in mice

2009 ◽  
Vol 133 (3) ◽  
pp. 437-446 ◽  
Author(s):  
Soichiro Fushimi ◽  
Tetsuya Ogino ◽  
Junko Hara ◽  
Tomohiro Takahata ◽  
Hiroshi Wakabayashi ◽  
...  
Keyword(s):  
T Cells ◽  
Concanavalin A ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling

scholarly journals A Role of Suppressor of Cytokine Signaling 3 (SOCS3/CIS3/SSI3) in CD28-mediated Interleukin 2 Production

2003 ◽  
Vol 197 (4) ◽  
pp. 425-436 ◽  
Author(s):  
Akira Matsumoto ◽  
Yoh-ichi Seki ◽  
Ryosuke Watanabe ◽  
Katsuhiko Hayashi ◽  
James A. Johnston ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Interleukin 2 ◽  
Sh2 Domain ◽  
Janus Kinase ◽  
Expression Level ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Cd28 Costimulation

Suppressor of cytokine signaling (SOCS)3 has been characterized as a negative feedback regulator in cytokine-mediated Janus kinase signal transducer and activator of transcription signaling. However, this study shows that T cells from transgenic mice expressing SOCS3 exhibit a significant reduction in interleukin (IL)-2 production induced by T cell receptor cross-linking when T cells are costimulated with CD28. Decreased protein expression in SOCS3+/− mice enhanced CD28-mediated IL-2 production, clearly indicating the correlation between expression level of SOCS3 and IL-2 production ability. The SOCS3 protein interacted with phosphorylated CD28 through its SH2 domain but not the kinase inhibitory region. In addition, a point mutation in the SOCS3 SH2 domain attenuated the inhibition of CD28 function in IL-2 promoter activation. Committed T helper (Th)2 cells exclusively expressed SOCS3 and production of Th2 cytokines, such as IL-4 and IL-5, was much less dependent on CD28 costimulation compared with interferon γ and IL-2 production in Th1 cells. Consistent with this notion, the expression level of SOCS3 in early T cell activation influenced the ability of IL-2 production induced by CD28 costimulation. Therefore, the SOCS3 may play an alternative role in prohibiting excessive progression of CD28-mediated IL-2 production.

scholarly journals Suppressor of Cytokine Signaling-1 Regulates Signaling in Response to Interleukin-2 and Other γc-dependent Cytokines in Peripheral T Cells

2003 ◽  
Vol 278 (25) ◽  
pp. 22755-22761 ◽  
Author(s):  
Ann L. Cornish ◽  
Mark M. Chong ◽  
Gayle M. Davey ◽  
Rima Darwiche ◽  
Nicos A. Nicola ◽  
...  
Keyword(s):  
T Cells ◽  
Interleukin 2 ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Peripheral T Cells

The Cytokine Signal Inhibitor Lnk Promotes αIIbβ3 Integrin Outside-In Signaling through β3 Tyrosine Phosphorylation in Platelets.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3651-3651
Author(s):  
Koji Eto ◽  
Hitoshi Takizawa ◽  
Satoshi Takaki ◽  
Hidekazu Nishikii ◽  
Atsushi Oda ◽  
...  
Keyword(s):  
Tyrosine Phosphorylation ◽  
Tyrosine Kinases ◽  
Adaptor Protein ◽  
Sh2 Domain ◽  
Cytokine Signaling ◽  
Adapter Protein ◽  
Clot Retraction ◽  
Hematopoietic Stem ◽  
Kinase Activation ◽  
C Terminus

Abstract Lnk is an SH2 domain-containing adapter protein that inhibits cytokine signaling. Lnk−/− mice exhibit a marked increase in numbers of hematopoietic stem cells, megakaryocytes and platelets, presumably due to the lack of negative regulation in thrombopoietin-mediated signals by Lnk. We previously reported that Lnk might play an unanticipated role in platelet integrin αIIbβ3 outside-in signaling. Lnk−/− platelets exhibited defects in full spreading on fibrinogen, clot retraction and formation of thrombi on collagen under flow conditions while they showed normal inside-out signaling (Blood, 106 (11):115a, 2005). However the mechanism(s) in which Lnk participates in αIIbβ3 outside-in signaling had not been elucidated. Here we report that in normal platelets Lnk forms a complex with c-Src, Syk, Fyn and adhesion and degranulation promoting adaptor protein (ADAP) but not SLP-76 in a manner dependent on αIIbβ3 ligation and Src kinase activation. c-Src-, but not Syk-, mediated tyrosine phosphorylation of C-terminus in Lnk appeared to be indispensable for the complex formation and Lnk-mediated function. Furthermore we have shown that Lnk is required for the association of Fyn to αIIbβ3 and for β3 subunit tyrosine phosphorylation while activation of non-receptor tyrosine kinases (c-Src and Syk) in proximity to αIIbβ3 is independent of Lnk. Thus, these results provide new insights into Lnk function and the mechanism by which Lnk contributes to integrin signaling in the adhesion responses of platelets.

Suppressor of cytokine signaling (SOCS) proteins are induced by IL-7 and target surface CD127 protein for degradation in human CD8 T cells

2016 ◽  
Vol 306-307 ◽  
pp. 41-52 ◽  
Author(s):  
Feras M. Ghazawi ◽  
Elliott M. Faller ◽  
Parmvir Parmar ◽  
Abdulkareem El-Salfiti ◽  
Paul A. MacPherson
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Target Surface ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Socs Proteins

Suppressor of cytokine signaling-1 in T cells and macrophages is critical for preventing lethal inflammation

Blood ◽  
2005 ◽  
Vol 106 (5) ◽  
pp. 1668-1675 ◽  
Author(s):  
Mark M. W. Chong ◽  
Donald Metcalf ◽  
Emma Jamieson ◽  
Warren S. Alexander ◽  
Thomas W. H. Kay
Keyword(s):  
T Cells ◽  
T Cell ◽  
Inflammatory Disease ◽  
Lymphoid Cells ◽  
Interleukin 12 ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Cytokine Network ◽  
Activated T Cells ◽  
Ifn Γ

Abstract The balance between pro- and anti-inflammatory cytokines modulates inflammation. Intracellular inhibitors of signaling, in turn, contribute to the negative regulation of cytokines. One of these inhibitors is suppressor of cytokine signaling-1 (SOCS-1). Socs1-/- mice die by 3 weeks of age with inflammation and fatty necrosis of the liver. Here, cre/loxP deletion of Socs1 was used to investigate the contribution of specific cells/tissues to inflammatory disease. Mice with SOCS-1 deficiency in myeloid and lymphoid cells, but not lymphoid alone, became ill at 50 to 250 days of age. These mice developed splenomegaly and T-cell/macrophage infiltration of many organs, including liver, lung, pancreas, and muscle. There were also abnormally high levels of the proinflammatory cytokines interferon γ (IFN-γ), tumor necrosis factor (TNF), and interleukin-12 (IL-12), and activated T cells circulating in these mice. Socs1null T cells were found to be hypersensitive to multiple cytokines, including IL-1, IL-2, and IL-12, resulting in IFN-γ production without requiring T-cell receptor (TCR) ligation. Additionally, Socs1null macrophages produced excessive amounts of IL-12 and TNF in response to other cytokines, including IFN-γ. A dysregulated cytokine network between T cells and macrophages is thus associated with this inflammatory disease. These findings indicate that SOCS-1 is critical in both T cells and macrophages for preventing uncontrolled inflammation. (Blood. 2005;106:1668-1675)

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