# NIH grant: Systematic mapping of innate immune signaling pathways (1R35GM161712-01) — retained record

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source: [us-gov-api](https://highsignal.app/data/us-gov-api) (us-gov-api:nih-reporter)  published 2026-07-01 00:00 ingested 2026-07-06 10:11

[original source ↗](https://reporter.nih.gov/project-details/1R35GM161712-01)

## retained text



```
NIH grant 1R35GM161712-01: Systematic mapping of innate immune signaling pathways
Institute: {'code': 'GM', 'abbreviation': 'NIGMS', 'name': 'National Institute of General Medical Sciences', 'admin_org_id': '12500024', 'admin_funding_url': ''}. PI: David Ezra Gordon. Award: $462000.
Start: 2026-07-01T00:00:00.
Abstract
 The Gordon Laboratory integrates high-throughput experimental genetics and proteomics to
build mechanistic models of biological functions, with a focus on innate immune signaling pathways.
Dysregulation of these pathways underlies numerous diseases, including inborn errors of immunity,
autoimmune disorders, and cancer. Our overarching vision is to develop capabilities for de novo
mapping of innate immune pathways, creating a generalizable framework for identifying key
components and complexes that drive innate immune functions.
 We leverage mass spectrometry-based proteomics to perform time-resolved analyses of post-
translational modifications and protein interaction networks, capturing the dynamic biochemical
changes underlying innate immune signaling. Our experimental genetics approaches employ CRISPR
pipelines in primary T cells, combined with in-vitro and in-vivo functional assays, to uncover causal
relationships and delineate the roles of specific pathways and protein complexes. In collaboration with
machine learning and bioinformatics groups, we integrate these datasets through graph network
analyses to construct mechanistic models of innate immune signaling.
 Over the next five years, we will implement and refine this framework through our studies of type
I and II interferons (IFNs) and interleukin-12 (IL-12). These cytokines orchestrate cell-autonomous
antiviral responses, drive inflammation, and regulate CD4+ Th1 cell differentiation—processes critical
for controlling viral spread and resolving infections. This work will advance fundamental knowledge of
innate immune pathways, providing insight into how these networks regulate CD4+ T cell function and
contribute to antiviral defense mechanisms.
```



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