SARS-CoV CYTOKINE STORM
Pathway ID: SIGNOR-SCCSView in NDEx
Description: Inflammation is an essential part of the immune response. Unfortunately, SARS-CoV-2 infection induces a massive and prolonged inflammatory responses in some patients, known as “cytokine storm”. Cytokine storm results from the effects of a combination of several immune-active molecules: interferons, chemokines, interleukins (eg Interferon γ, interleukin IL-1B, IL-6, IL-12, CXCL10, CCL2 and TNF-alpha) represent the main components involved in its development. The uncontrolled production and secretion of these factors cause a massive and generalized inflammatory response that could culminates into ARDS (acute respiratory distress syndrome) or acute lung injury, two clinical conditions with high mortality rate. Efficent control of the cytokine storm is the key to improving the treatment success and reducing the mortality rate of patients with COVID-19.
Curated by: Marta Iannuccelli
Description: Inflammation is an essential part of the immune response. Unfortunately, SARS-CoV-2 infection induces a massive and prolonged inflammatory responses in some patients, known as “cytokine storm”. Cytokine storm results from the effects of a combination of several immune-active molecules: interferons, chemokines, interleukins (eg Interferon γ, interleukin IL-1B, IL-6, IL-12, CXCL10, CCL2 and TNF-alpha) represent the main components involved in its development. The uncontrolled production and secretion of these factors cause a massive and generalized inflammatory response that could culminates into ARDS (acute respiratory distress syndrome) or acute lung injury, two clinical conditions with high mortality rate. Efficent control of the cytokine storm is the key to improving the treatment success and reducing the mortality rate of patients with COVID-19.
Curated by: Marta Iannuccelli
44 Seed Entities
Organism: | Name | Primary ID |
---|---|
IL10 | P22301 |
IL10RA | Q13651 |
IL6R | P08887 |
S | P59594 |
JUN | P05412 |
3a | P59632 |
IL1R1 | P14778 |
T_cell_activation | SIGNOR-PH73 |
ARDS | SIGNOR-PH128 |
IL1RN | P18510 |
STAT3 | P40763 |
6 | P59634 |
CCL2 | P13500 |
IFNB1 | P01574 |
IFNGR2/INFGR1 | SIGNOR-C142 |
IFNA1 | P01562 |
TLR2 | O60603 |
Macrophage_activation | SIGNOR-PH126 |
JAK1 | P23458 |
TNF | P01375 |
IFNG | P01579 |
IL1B | P01584 |
IRF7 | Q92985 |
3b | P59633 |
NfKb-p65/p50 | SIGNOR-C13 |
N | P59595 |
EIF2AK2 | P19525 |
CCL7 | P80098 |
IL6ST | P40189 |
Immune_response | SIGNOR-PH17 |
chloroquine | CHEBI:3638 |
Host translation inhibitor nsp1 | P0C6X7-PRO_0000037309 |
Inflammation | SIGNOR-PH12 |
Tocilizumab | DB06273 |
IL18 | Q14116 |
ISGF3 complex | SIGNOR-C124 |
AP1 | SIGNOR-C154 |
Uridylate-specific endoribonuclease | P0C6X7-PRO_0000037321 |
IL6 | P05231 |
IL12A | P29459 |
CXCL8 | P10145 |
CXCL10 | P02778 |
IFNAR | SIGNOR-C243 |
STAT1 | P42224 |