Modulating Endothelial Venuleness for Tissue-Specific Inflammation Control
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Solution Overview
Problem
Current anti-inflammatory and onco-immunotherapy drugs affect inflammation levels in a non-targeted manner, leading to severe adverse effects on healthy tissues, as they either increase or decrease inflammation without specificity to diseased tissues.
Innovation Solution
Methods are developed to modulate inflammation by reducing or increasing the venuleness of endothelial cells (ECs) through targeted gene expression modulation, using agents such as polypeptides, small molecules, nucleic acids, and viral vectors to specifically target ECs in specific tissues, thereby reducing inflammation in inflammatory diseases or increasing leukocyte recruitment in cancers.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If current anti-inflammatory drugs are used to decrease inflammation, then inflammation levels are reduced, but severe adverse effects occur on healthy non-target tissues
Solution Approach 1:
The patent applies local quality by making the anti-inflammatory effect tissue-specific through modulation of venuleness in selected tissues only. By targeting specific endothelial cell populations in diseased tissues and leaving healthy tissues unaffected, the treatment achieves localized inflammation reduction without systemic adverse effects on healthy non-target tissues.
Solution Approach 2:
The patent segments the vascular endothelium into different populations based on venuleness characteristics in different tissues. By selectively modulating venuleness in specific tissue beds (e.g., inflamed tissues) while preserving it in healthy tissues, the treatment achieves spatial segmentation of the anti-inflammatory effect, delivering therapy only where needed.
2Reliability
If current onco-immunotherapy drugs are used to increase inflammation, then leukocyte recruitment is enhanced, but severe adverse effects occur on healthy non-target tissues
Solution Approach 1:
The patent applies local quality by making the pro-inflammatory effect tissue-specific through selective modulation of venuleness in tumor tissues only. By targeting specific endothelial cell populations in cancerous tissues and leaving healthy tissues unaffected, the treatment achieves localized leukocyte recruitment enhancement without systemic adverse effects on healthy non-target tissues.
Solution Approach 2:
The patent segments the vascular endothelium into different populations based on venuleness characteristics in different tissues. By selectively modulating venuleness in specific tissue beds (e.g., tumor tissues) while preserving it in healthy tissues, the treatment achieves spatial segmentation of the immunotherapeutic effect, delivering enhanced leukocyte recruitment only where needed for cancer treatment.
3Adaptability or versatility
If non-targeted anti-inflammatory or onco-immunotherapy drugs are used, then inflammation levels are modulated, but tissue-specificity is lost
Solution Approach 1:
The patent resolves this contradiction by making inflammation modulation tissue-specific through selective venuleness modulation. By targeting specific endothelial cell populations in diseased tissues and using tissue-specific markers or delivery mechanisms, the treatment achieves both adaptability in inflammation modulation and precision in tissue targeting simultaneously.
Solution Approach 2:
The patent uses venuleness modulation as an intermediary mechanism to achieve tissue-specific inflammation control. By modulating the venuleness of endothelial cells in selected tissues through specific agents or methods, the treatment creates a bridge between the desire for broad inflammation modulation capability and the need for precise tissue-specific targeting, allowing controlled delivery of anti-inflammatory or pro-inflammatory effects only where venuleness is modulated.
Data Source
AI summary
Disclosed herein are genes which are differentially expressed in venule endothelial cells (V-ECs) compared to non-venule endothelial cells (NV-ECs), and methods and compositions relating to those genes. In particular, described herein are methods of reducing the venuleness of endothelial cells (ECs) for treating inflammatory diseases, and methods of increasing the venuleness of ECs for treating cancers.