LIGHT and its signaling receptors, herpesvirus entry mediator (TNFRSF14), and lymphotoxin β receptor, form an immune regulatory network
First-pass extracted concept
LIGHT regulatory network
Candidate: toolkit item1 source documents3 linked claims
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Aliases
LIGHT network, LIGHT signaling network
Evidence Snippets
Supporting Sources
Linked Claims
Dysregulation of the LIGHT network is a disease-driving mechanism in autoimmune and inflammatory reactions in barrier organs, including COVID-19 pneumonia and inflammatory bowel diseases.
Quoted textsource-backed
Accumulating evidence from infectious diseases points to the dysregulation of the LIGHT network as a disease-driving mechanism in autoimmune and inflammatory reactions in barrier organs, including coronavirus disease 2019 pneumonia and inflammatory bowel diseases.
LIGHT, herpesvirus entry mediator, lymphotoxin β receptor, B and T lymphocyte attenuator, and CD160 form an immune regulatory network.
Quoted textsource-backed
LIGHT and its signaling receptors, herpesvirus entry mediator (TNFRSF14), and lymphotoxin β receptor, form an immune regulatory network with two co-receptors of herpesvirus entry mediator, checkpoint inhibitor B and T lymphocyte attenuator, and CD160.
Understanding the LIGHT regulatory network can guide therapeutic development and supports further investigation of target-modifying therapeutics for disease intervention.
Quoted textsource-backed
Deciphering the fundamental features of this network reveals new understanding to guide therapeutic development. Recent clinical results warrant further investigation of the LIGHT regulatory network and application of target-modifying therapeutics for disease intervention.