AcvR1c Inhibitor Modulation of Treg Function
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Solution Overview
Problem
Regulatory T cells (Tregs) pose a barrier to effective anti-tumor immunity, as they suppress aberrant immune responses but also hinder the immune system's ability to target cancer cells.
Innovation Solution
Targeting Activin receptor 1C (AcvR1c) to modulate Treg function, activity, or proliferation, using inhibitors such as antibodies or small molecules that specifically bind to AcvR1c, thereby blocking Activin binding and reducing Treg suppressive functions.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If Treg cells are used to suppress aberrant immune responses, then immune homeostasis is maintained, but anti-tumor immunity is hindered
Solution Approach 1:
The patent applies local quality by differentiating the suppressive function of Treg cells based on tissue location. Treg cells are described as maintaining immune homeostasis in peripheral tissues while being depleted or inhibited in tumor microenvironments. This spatial differentiation allows the system to preserve beneficial suppressive functions elsewhere while removing harmful suppressive effects at tumor sites, thereby resolving the contradiction between maintaining immune homeostasis and enabling anti-tumor immunity.
Solution Approach 2:
The patent extracts the harmful suppressive function of Treg cells from the tumor microenvironment through various depleting and inhibiting therapies. By selectively removing or inhibiting Treg cells in tumor tissues while preserving them in peripheral tissues, the invention separates the beneficial homeostatic function from the harmful anti-tumor barrier, enabling effective cancer treatment without compromising overall immune stability.
2Reliability
If TGF-β/IL-2 signaling pathways are activated to induce Treg cells, then Foxp3 expression and suppressive function are enhanced, but uncontrolled immune suppression occurs
Solution Approach 1:
The patent implements feedback control by monitoring and regulating Treg cell induction through TGF-β/IL-2 signaling pathways. The system uses feedback mechanisms to ensure that Treg cells are induced only when and where needed, preventing excessive or uncontrolled immune suppression. This regulated induction allows the system to achieve sufficient Treg function for homeostasis while avoiding harmful over-suppression.
Solution Approach 2:
The patent applies dynamics by making the Treg induction process adjustable and context-dependent. The TGF-β/IL-2 signaling pathways are dynamically regulated based on local immune conditions, allowing the system to adapt the level of Treg induction to match actual needs. This dynamic control enables the system to achieve optimal Treg function when required while preventing excessive suppression in inappropriate contexts.
3Object-generated harmful factors
If AcvR1c is blocked to reduce Treg suppressive function, then anti-tumor immunity is enhanced, but Treg-mediated immune homeostasis is disrupted
Solution Approach 1:
The patent applies local quality by targeting AcvR1c specifically in the tumor microenvironment rather than systemically. By localizing the blockade of AcvR1c to tumor tissues, the system reduces Treg suppressive function where it is harmful to anti-tumor immunity while preserving Treg-mediated immune homeostasis in peripheral tissues. This spatially-specific approach resolves the contradiction by differentiating between local and system-wide effects.
Solution Approach 2:
The patent extracts the harmful AcvR1c signaling activity from the tumor microenvironment through targeted blockade therapies. By removing or inhibiting AcvR1c specifically in tumor tissues, the system separates the harmful Treg suppressive function from the beneficial immune homeostasis function, allowing the latter to persist while eliminating the former.
Applied Scientific Principles
This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.
Function Achieved in This Case
The blockade of AcvR1c enhances the effectiveness of anti-tumor vaccines and reduces Treg-mediated immune suppression, leading to improved anti-tumor immunity and potentially effective cancer treatment.
Implementation Method 1
the inhibitor comprises an antibody or antigen binding fragment which specifically binds to AcvR1c and inhibits Activin binding to the AcvR1c
Implementation Method 2
This occurs through the activation of the TGF-β/IL-2 signaling pathways (5). TGF-β is a potent inducer of Foxp3 expression in vitro and in vivo and members of the SMAD family of signaling molecules serve as critical facilitators and regulators of TGF-β-initiated signaling events and downstream gene activation (6)
Data Source
AI summary
Compositions and methods for the prevention and treatment of cancer and autoimmune diseases are provided which include agents which modulate the expression or function of Activins and Activin receptors. Compositions in the treatment of cancer include blockade Activin receptor 1c (AcvR1c). In one aspect, a method of modulating regulatory T cells (Tregs) in vitro or in vivo, comprises a) contacting a cell in vitro or administering to a subject an effective amount of Activin and/or an agent for modulating of Activin expression or function and/or an agent for modulating or blocking an Activin receptor (AcvR) expression or function; and b) modulating Tregs in vitro or in vivo.