pG6b Modulators for Selective Immune Response Control
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Solution Overview
Problem
Current therapies lack effective agents to modulate immune responses, particularly in autoimmune disorders and cancer, where autoreactive T cells and insufficient immune responses to pathogens or tumor antigens are concerns, and there is a need for agents that can enhance or inhibit immune reactions without compromising immune function.
Innovation Solution
Development of polypeptides and antibodies targeting pG6b, a member of the CD28 family, to modulate lymphocyte activity by interfering with or mimicking its signaling, thereby influencing T cell and B cell activation, proliferation, and antibody production.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Object-affected harmful factors
If agents are used to inhibit or eliminate autoreactive lymphocytes, then autoimmune responses are reduced, but the immune system's ability to defend against pathogens may be compromised
Solution Approach 1:
The patent applies local quality by selectively targeting pG6b signaling pathways in specific cell types (T cells and B cells) to inhibit autoreactive responses while preserving overall immune function. The modulators are designed to act locally on the costimulatory pathway rather than broadly suppressing the entire immune system, thus reducing harmful autoreactive activity without compromising pathogen defense capability.
Solution Approach 2:
The patent utilizes parameter changes by modulating the activity level of pG6b and its interacting molecules (such as B7-1, B7-2, CD28, and CTLA-4) to shift the balance between autoreactive and protective immune responses. By changing the signaling parameters of costimulation, the system can selectively inhibit harmful responses while maintaining beneficial immune functions.
2Power
If agents are used to expand tumor-specific T cell populations, then tumor attack capability is enhanced, but the complexity of immune modulation increases
Solution Approach 1:
The patent extracts and isolates the specific pG6b costimulatory pathway as a target for immunomodulation. By focusing on this specific molecular interaction rather than attempting to modulate the entire immune system, the complexity of immune modulation is reduced while still achieving enhanced tumor attack capability through targeted expansion of tumor-specific T cells.
Solution Approach 2:
The patent employs pG6b modulators as intermediary agents that facilitate the expansion and activation of tumor-specific T cells. These modulators act as mediators between the tumor antigen and the T cell response, simplifying the overall immune modulation process while enhancing tumor attack capability through controlled T cell proliferation and differentiation.
3Reliability
If adjuvants are administered to enhance immune response to antigen, then protection against disease is improved, but the risk of excessive immune activation increases
Solution Approach 1:
The patent applies the inversion principle by using pG6b modulators to enhance protective immune responses against tumors and pathogens while simultaneously inhibiting harmful autoreactive responses. This inverted approach allows the same molecular pathway to be activated for beneficial purposes (tumor rejection, pathogen clearance) while being inhibited for harmful purposes (autoreactivity), thus improving protection without causing excessive immune activation.
Solution Approach 2:
The patent utilizes dynamics by creating a balanced, adjustable immune response through pG6b modulation. The system can dynamically shift the balance between protective and harmful immune responses based on the specific disease context, allowing enhancement of protection against tumors and pathogens while preventing excessive activation through controlled modulation of costimulatory signals.
Data Source
AI summary
The present invention provides a newly identified CD28 family member that functions as lymphocyte inhibitory receptor termed pG6b, which is expressed on T cells. Methods and compositions for modulating pG6b-mediated negative signaling and interfering with the interaction of its counter-receptor for therapeutic, diagnostic, and research purposes are also provided.