| + |
T_cell_activation | up-regulates 
|
ARDS |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261022 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32446778 |
The presence of SARS-CoV-2 in the lung induces an uncontrolled generalized immune response. Several immune cells (like T-lymphocytes, macrophages and dendritic cells) sustain the impressive secretion of cytokines and chemokines ultimately leading to acute respiratory distress syndrome. These data clearly indicate that, in SARS-CoV in-fection, ARDS is the ultimate result of a cytokine storm. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
T_cell_activation | up-regulates quantity
|
IL17A |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263819 |
|
|
Homo sapiens |
Helper T-lymphocyte |
| pmid |
sentence |
| 32454942 |
interferon gamma- (IFNγ-) and interleukin-17- (IL-17-) secreting CD4+ T cells are believed to be the pathogenic initiators of MS [22], and in MS patients, the increased production of either IFNγ or IL-17 is associated with pathology |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
IL12A | up-regulates
|
T_cell_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260966 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10653850 |
IL-12 Synergizes With IL-18 or IL-1beta for IFN-gamma Production From Human T Cells. IL-12 and IL-18 acted in a synergistic manner for the development of T cells into IFN-γ-producing cells without their TCR. Here we show that IL-12 and IL-1beta synergistically induce T cells to proliferate and produce IFN-gamma without their TCR engagement. IL-12 stimulation induced an increase in the proportion of T cells positive for IL-18R engagement. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
MAP4K1 | down-regulates 
|
T_cell_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-274563 |
|
|
Homo sapiens |
JURKAT Cell |
| pmid |
sentence |
| 17353368 |
Thus, our study reveals the mechanism of a novel negative feedback loop initiated from SLP-76 to modulate signal intensity during T cell activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection |
| + |
STAT3 | up-regulates
|
T_cell_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263821 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32454942 |
IL-1β, an inflammatory cytokine primarily expressed in activated macrophages, monocytes, and microglia, significantly contributes to MS development. IL-1β promotes differentiation of T cells into Th17 cells via the STAT3 pathway and thereby promotes and aggravates the inflammatory environment in the CNS |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | EBV infection, Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
Class II MHC:Antigen | up-regulates
|
T_cell_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267873 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 31810556 |
Once they are formed, peptide/MHC class II molecules complexes are very stable and allow for sustained antigen presentation increasing the chances to encounter the matching CD4+ T lymphocytes. Once CD4+ T cells have become acti- vated, they in turn trigger macrophages to eliminate pathogens that have been previously internalized, and B lymphocytes to produce pathogen- specific antibodies. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | T cell activation |
| + |
IL18 | up-regulates
|
T_cell_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260965 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10653850 |
IL-12 Synergizes With IL-18 or IL-1beta for IFN-gamma Production From Human T Cells. IL-12 and IL-18 acted in a synergistic manner for the development of T cells into IFN-γ-producing cells without their TCR. Here we show that IL-12 and IL-1beta synergistically induce T cells to proliferate and produce IFN-gamma without their TCR engagement. IL-12 stimulation induced an increase in the proportion of T cells positive for IL-18R engagement. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
CBM | up-regulates
|
T_cell_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-276297 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 35230873 |
The CBM complex not only induces a productive immune response in activated effector T cells but also controls peripheral tolerance by promoting the development and function of regulatory T (Treg) cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
T_cell_activation | up-regulates quantity
|
IFNG |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260967 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10653850 |
IL-12 Synergizes With IL-18 or IL-1beta for IFN-gamma Production From Human T Cells. IL-12 and IL-18 acted in a synergistic manner for the development of T cells into IFN-γ-producing cells without their TCR. Here we show that IL-12 and IL-1beta synergistically induce T cells to proliferate and produce IFN-gamma without their TCR engagement. IL-12 stimulation induced an increase in the proportion of T cells positive for IL-18R engagement. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263818 |
|
|
Homo sapiens |
Helper T-lymphocyte |
| pmid |
sentence |
| 32454942 |
interferon gamma- (IFNγ-) and interleukin-17- (IL-17-) secreting CD4+ T cells are believed to be the pathogenic initiators of MS [22], and in MS patients, the increased production of either IFNγ or IL-17 is associated with pathology |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
Class I MHC:Antigen | up-regulates
|
T_cell_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267775 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 31810556 |
High-affinity peptide/MHC class I complexes that successfully pass the aforementioned “quality controls” will be transported through the Golgi apparatus to the cell membrane to elicit antigen-specific CD8+ T cell responses. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | T cell activation |
| + |
IL6ST | up-regulates
|
T_cell_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261028 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32234467 |
Interleukin-6 (IL-6) is an important member of the cytokine network and plays a central role in acute inflammation. IL-6 binds to its receptor IL-6R to form a complex, and then binds to the membrane protein gp130 to initiate intracellular signal transduction. IL-6 is the terminal helper factor of cytotoxic T lymphocyte (CTL), which can induce CTL activity and make immature thymocytes develop into CTL. In addition, IL-6 is a pro-inflammatory regulator of T cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis, SARS-CoV CYTOKINE STORM |
| + |
NFATC1 | up-regulates activity
|
T_cell_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252344 |
|
|
|
|
| pmid |
sentence |
| 10358178 |
The transcription factor NF-ATc that controls gene expression in T lymphocytes and embryonic cardiac cells is expressed in three prominent isoforms. |
|
| Publications: |
1 |
| Pathways: | T cell activation |
3.0
T_cell_activation