Activated Fibroblasts for IL-17 Suppression in Chronic Inflammation
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Solution Overview
Problem
Existing treatments for inflammation associated with excessive production of inflammatory cytokines, such as IL-17, are inadequate in effectively suppressing the inflammatory response and preventing chronic inflammation in various autoimmune and inflammatory diseases.
Innovation Solution
Utilizing fibroblasts that express interleukin-3 receptor, CD73, and CD56, activated by agents like oxytocin, to inhibit IL-17 production and reduce the generation of Th17 cells, thereby reducing the inflammatory response through the production of anti-inflammatory cytokines IL-10, IL-35, and IL-37.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If existing treatments are used to suppress inflammation, then some inflammatory response is reduced, but they are inadequate in effectively suppressing IL-17 production and preventing chronic inflammation
Solution Approach 1:
The patent modifies the functional state of fibroblasts by activating them with specific agents (oxytocin, bradykinin, histamine, or ionizing radiation) to change their cytokine production parameters. This activation transforms fibroblasts from a state that produces pro-inflammatory cytokines to a state that produces anti-inflammatory cytokines (IL-10, IL-35, IL-37), thereby effectively suppressing IL-17 production and preventing chronic inflammation in autoimmune diseases
Solution Approach 2:
The patent uses activated fibroblasts as intermediary cells that mediate the suppression of IL-17 production by Th17 cells. These activated fibroblasts serve as a bridge between the administered activation agents and the target immune cells, releasing anti-inflammatory cytokines that indirectly suppress the harmful inflammatory response without directly targeting the immune cells
2Reliability
If fibroblasts are activated to produce anti-inflammatory cytokines, then IL-17 production is suppressed, but the complexity of activation methods increases
Solution Approach 1:
The patent demonstrates that multiple different activation agents (oxytocin, bradykinin, histamine, ionizing radiation) can all achieve the same therapeutic effect of activating fibroblasts to produce anti-inflammatory cytokines. This multi-functionality provides flexibility in treatment protocols and allows clinicians to choose from various activation methods based on patient-specific factors, thereby managing complexity while maintaining reliable IL-17 suppression
3Reliability
If multiple cytokines are targeted for suppression, then comprehensive inflammation control is achieved, but treatment specificity becomes more difficult to maintain
Solution Approach 1:
The patent achieves comprehensive inflammation control through a localized mechanism where activated fibroblasts produce multiple anti-inflammatory cytokines (IL-10, IL-35, IL-37) at the specific site of inflammation. This local production of multiple cytokines targets the inflammatory response precisely where needed, maintaining treatment specificity while achieving comprehensive suppression of IL-17 and other pro-inflammatory mediators in the affected tissue microenvironment
Data Source
Figure 1
AI summary
Embodiments of the disclosure concern reducing deleterious effects of inflammatory cytokines, such as interleukin-17, by providing to an individual with inflammation or at risk for inflammation an effective amount of fibroblasts and/or fibroblast derivatives thereof that reduce production of IL-17 from immune cells, that suppress responsiveness of cells to IL17, and/or that suppress generation of Th17 cells.