Soluble CD52 Glycoprotein T-Cell Suppression
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Solution Overview
Problem
Current methods lack effective mechanisms to suppress T-cell activation, particularly in autoimmune diseases and conditions mediated by effector T-cell function, and there is a lack of specific markers and understanding of human regulatory T-cell function.
Innovation Solution
The use of soluble CD52 glycoprotein or fusion proteins, which are capable of suppressing effector T-cell function by binding to Siglec-10, thereby reducing immune responses and inducing tolerance to autoantigens, is proposed, along with methods for detecting susceptibility to diseases mediated by effector T-cell function.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If soluble CD52 glycoprotein is used to suppress T-cell activation, then immune response suppression is improved, but specificity of Treg cell identification deteriorates due to lack of specific cell surface markers
Solution Approach 1:
The patent uses soluble CD52 glycoprotein as an intermediary mediator to suppress T-cell activation. Instead of directly using cell surface markers for identification, the invention employs the soluble form of CD52 that can bind to and suppress effector T-cells, thereby resolving the contradiction between achieving reliable immune suppression and dealing with the complexity of specific marker identification
Solution Approach 2:
The invention changes the state of CD52 from membrane-bound to soluble form. This parameter change allows CD52 to function as a soluble mediator that can suppress T-cell activation without requiring specific cell surface marker identification, thus improving immune response suppression while avoiding the complexity of marker-specific approaches
2Reliability
If CD4+CD25+ Treg cells are used for suppression, then suppression mechanism is improved, but understanding of human Treg cell function deteriorates due to limited knowledge of in vivo function
Solution Approach 1:
The patent extracts the suppressive function from the complex CD4+CD25+ Treg cell population and isolates it into a specific soluble mediator (soluble CD52). This extraction allows the suppressive mechanism to be studied and applied independently, improving our understanding of the actual in vivo suppression function without the confounding variables of polyspecific Treg populations
3Adaptability or versatility
If polyspecific Treg cell populations are used, then broad suppression is improved, but antigen-specific tolerance deteriorates due to inability to target specific autoantigens
Solution Approach 1:
The patent segments the broad suppressive function into antigen-specific components by using soluble CD52 that can be combined with specific autoantigens. This segmentation allows the system to maintain broad suppressive capability while also achieving antigen-specific tolerance, resolving the contradiction between versatility and reliability in different therapeutic contexts
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 soluble CD52 glycoprotein effectively suppresses T-cell activation and immune responses, potentially treating autoimmune diseases and conditions by inducing tolerance to autoantigens, and diagnosing susceptibility through CD52 level detection.
Implementation Method 1
capable of suppressing effector T-cell function by binding to Siglec-10
Data Source
Figure 1A~1B
Figure 2A~2A3
Figure 2B~2C
AI summary
The present disclosure relates to a soluble CD52 glycoprotein and its use in treating diseases regulated by effector T-cells, for example autoimmune diseases such as type 1 diabetes. The present disclosure also relates to fusion proteins comprising the soluble glycoprotein, to cells expressing high levels of CD52, and to diagnostic methods based on the detection of CD52 expression levels in a subject.