Derepression Of Interferon Stimulated Genes For Enhancing Protection In Autoinflammatory Reactions Including Those During Respiratory Infections.

Technology Description

UNMET NEED: Severe COVID-19 patients experience immune system dysfunction, including suppression of protective interferon-stimulated gene (ISG)-expressing immune populations, which contributes to disease progression and mortality. Current treatments fail to address these dysregulated immune responses.

TECHNOLOGY: Researchers at UCSF have uncovered a novel mechanism wherein overactive antibody responses in severe COVID-19 patients inhibit interferon-stimulated protective immune states by engaging Fc receptors (FcRs) on immune cells. This discovery highlights the role of antibody-driven immune suppression in severe cases and offers new targets for immunotherapy to restore effective antiviral defense mechanisms. Developmental status: preclinical proof-of-concept achieved.

COMPETITIVE ADVANTAGE:

• Identifies novel immune dysfunction: Severe COVID-19 patients produce antibodies that inhibit ISG-expressing immune cells, critical for antiviral defense.
• Fc receptor signaling mechanism: Reveals that antibody-mediated signaling through inhibitory Fc receptors (CD32b) blocks interferon responses, leading to immune suppression.
• Therapeutic potential: Suggests targeted approaches to restore immune function, such as Fc receptor blockade, B cell-modulating therapies, or IVIG to compete with pathogenic antibodies.
• Broad applicability: Findings may extend to other viral infections with similar antibody-driven immune suppression, paving the way for new immunotherapy strategies.

Patent Status

Patent Pending