IL12Rβ1 Splice Variant Quantification for Immune Response Control
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Solution Overview
Problem
Current methods lack the ability to effectively augment or inhibit type-1 cellular immune responses depending on the circumstances, as they do not provide a means to quantify or manipulate the ratio of IL12Rβ1 cDNA and its splice variant, which is crucial for managing immune reactions to pathogens like Mycobacterium tuberculosis.
Innovation Solution
A vaccine formulation comprising an antigen and the IL12Rβ1 isoform 2, along with methods to quantify the ratio of IL12Rβ1 cDNA and its splice variant, and the administration of peptide isoforms or inhibitors to enhance or suppress type-1 cellular immune responses, using PCR primer sets and fluorescent-conjugated primers for detection and siRNA or antibodies for modulation.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Measurement precision
If current methods are used to manage immune responses, then general immune modulation is possible, but the ability to specifically quantify and manipulate the ratio of IL12Rβ1 cDNA and its splice variant is lacking
Solution Approach 1:
The invention segments the IL12Rβ1 gene expression into distinct measurable components by developing PCR primer sets that specifically target and differentiate between the full-length cDNA and the splice variant. This segmentation enables precise quantification of the ratio between the two forms, transforming the complex immune response management into measurable, controllable parameters through molecular biology techniques.
2Reliability
If the IL12Rβ1 splice variant is administered to augment immune response, then type-1 cellular immune response is enhanced, but the complexity of monitoring and controlling the response increases
Solution Approach 1:
The invention implements feedback mechanisms by developing quantitative PCR assays that continuously monitor the ratio of IL12Rβ1 cDNA to splice variant in patient samples. This feedback allows clinicians to adjust the administration of the splice variant or associated therapies in real-time, optimizing immune response augmentation while controlling complexity through data-driven decision making.
3Object-affected harmful factors
If inhibitors are used to suppress type-1 cellular immune response, then inflammatory responses are reduced, but the precision of targeting specific immune pathways is limited
Solution Approach 1:
The invention applies local quality by developing inhibitors that specifically target the IL12Rβ1 splice variant or its interacting partners, rather than using broad-spectrum immunosuppressants. The PCR-based quantification methods enable precise identification of patients who would benefit from this localized inhibition, improving both the specificity of therapy and the reduction of harmful inflammatory responses.
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
This approach allows for the augmentation or inhibition of type-1 cellular immune responses, enhancing vaccine efficacy or reducing inflammatory responses by specifically targeting the IL12Rβ1 isoform 2, thereby improving immune reaction management.
Implementation Method 1
amplifying the cDNAs with the PCR primer set
Implementation Method 2
labeling the products of the PCR amplification with the fluorescent-conjugated primer and detecting the labeled PCR products
Data Source
AI summary
The present invention describes compositions for both diagnostic and therapeutic applications. In one embodiment, the present invention contemplates a vaccine formulation comprising an antigen and IL12Rβ1 isoform 2. In some embodiments, this invention relates to a method of quantifying the ratio of IL12Rβ1 transcript and a splice variant thereof in a sample, including but not limited to at the cDNA level. In other embodiments, this invention relates to a method of augmenting an immune response by administering, inhibiting and/or inducing IL12Rβ1 isoform 2.