CD38 Polypeptide Composition for Immune Tolerance in Autoimmune Disease
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Solution Overview
Problem
Current treatments for autoimmune diseases, such as rheumatoid arthritis and inflammatory bowel disease, have limitations including immunosuppression side effects, microbial susceptibility, and impact on immune homeostasis, necessitating the development of more targeted and effective therapeutic agents.
Innovation Solution
A polypeptide with an amino acid sequence represented by X1-L-Q-C-V-K-N-P-E-X2-X3-S-C, where X1, X2, and X3 vary, is used to induce immune tolerance by reducing TNF-α, IFN-γ, and IL-17 levels, and increasing Treg cells, formulated in a pharmaceutical composition with a nucleic acid molecule, vector, or isolated cell for administration.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If adrenocortical hormone drugs and immunosuppressants are used to treat autoimmune diseases, then the autoimmune disease symptoms are suppressed, but the body's overall immunity is lowered and microbial susceptibility increases
Solution Approach 1:
The patent uses soluble CD38 as an intermediary substance that selectively modulates the immune system. CD38 acts as a mediator that targets specific immune pathways (TNF-α, IFN-γ, IL-17) without broadly suppressing overall immunity, thus resolving the contradiction between disease suppression and microbial susceptibility.
Solution Approach 2:
The patent applies local quality by targeting specific immune components (TNF-α, IFN-γ, IL-17) and cell types (Treg cells) rather than broadly suppressing the entire immune system. This selective modulation suppresses autoimmune disease activity in specific areas while preserving overall immune function and microbial defense.
2Reliability
If TNF-α inhibitors are used to treat autoimmune diseases, then the disease selectivity and effectiveness are improved, but susceptibility to microbial infections increases during long-term treatment
Solution Approach 1:
The patent changes the parameter of immune modulation by using soluble CD38 instead of TNF-α inhibitors. CD38 modulates multiple cytokine parameters (TNF-α, IFN-γ, IL-17) simultaneously, achieving disease selectivity while maintaining broader immune function that protects against microbial infections.
Solution Approach 2:
The patent employs a composite approach by targeting multiple immune pathways and cell types simultaneously through CD38. This composite modulation of immune responses (combining effects on TNF-α, IFN-γ, IL-17, and Treg cells) provides both disease selectivity and microbial defense, unlike single-pathway TNF-α inhibitors.
3Duration of action of stationary object
If steroids and immunosuppressants are used for long-term treatment, then the autoimmune disease is controlled, but the body's overall immunity is compromised
Solution Approach 1:
The patent enables the immune system to regulate itself through CD38-mediated modulation. By enhancing Treg cell function and balancing cytokine production, the immune system achieves long-term disease control through its own regulatory mechanisms rather than relying on external immunosuppressive drugs that compromise overall immunity.
Solution Approach 2:
The patent implements feedback mechanisms through CD38, which modulates immune responses based on the body's actual needs. The soluble CD38 form provides feedback regulation of cytokine production and Treg cell activity, enabling sustained disease control while maintaining appropriate overall immune function without the need for long-term broad immunosuppression.
Data Source
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AI summary
The present disclosure relates to a polypeptide including a fragment of CD38. In addition, the present disclosure relates to a composition containing CD38 or a fragment thereof for preventing or treating autoimmune diseases. The CD38 or the fragment thereof, according to the present disclosure, increases regulatory T-cells (Tregs) and alleviates various symptoms of autoimmune diseases, and thus can be used as an agent for preventing or treating autoimmune diseases.