| + |
Macrophage_activation | up-regulates quantity 
|
IL18 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260964 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 10653850 |
IL-18, originally described as IFN-γ-inducing factor, is secreted from activated macrophages and Kupffer cells (1–3). The major activity associated with this cytokine is induction of IFN-γ production from CD4+ Th1 cells, T cells, B cells and NK cells, especially in collaboration with IL-12. IL-12 and IL-18 acted in a synergistic manner for the development of T cells into IFN-γ-producing cells without their TCR engagement. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
CCL7 | up-regulates
|
Macrophage_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260850 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
Macrophage_activation | up-regulates quantity
|
CCL7 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260963 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
CCL2 | up-regulates
|
Macrophage_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260849 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
Macrophage_activation | up-regulates quantity
|
CCL2 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260962 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
IFNAR | up-regulates
|
Macrophage_activation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260848 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 32283152 |
The rapid replication of SARS-CoV in BALB/c mice induces the delayed release of IFN-α/β, which is accompanied by the influx of many pathogenic inflammatory mononuclear macrophages. The accumulated mononuclear macrophages receive activating signals through the IFN-α/β receptors on their surface and produce more monocyte chemoattractants (such as CCL2, CCL7, and CCL12), resulting in the further accumulation of mononuclear macrophages. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
Macrophage_activation | up-regulates
|
ARDS |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261021 |
|
|
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 |
3.0
Macrophage_activation