Project Overview

Autoimmune diseases arise from a cascade of aberrant cell-cell interactions in which the immune system mistakenly targets self-tissue, driving chronic inflammation and tissue destruction. Despite the central role these interactions play, they remain poorly understood, limiting the number of available interventions. This project addresses that gap by developing a novel cell-labeling tool that enables immune cells to permanently and genetically mark the neighboring cells they contact — capturing interaction partners in real time and allowing researchers to track their long-term fate. The tool will first be applied to characterize the interaction partners of skin-resident T cells in a mouse model of psoriasis, with the ultimate goal of identifying strategies to evict these cells from their niche and prevent disease recurrence.

Impact & Innovation

Observing immune interactions as they happen

 

This project creates a first-of-its-kind tool that permanently labels the cell partners of immune interactions in living tissue — transforming how researchers study the roots of autoimmune disease.

  • Fills a critical methodological gap: for the first time enabling direct, in vivo capture of immune cell contact networks in living tissue
  • Broadly applicable across autoimmune conditions; already in discussion for biotech licensing through NYU’s technology office
  • Advances the Consortium’s Shared Mechanisms Across Autoimmune Diseases pillar, generating a platform tool for studying immune cell interactions across multiple disease models
Research Approach

A framework designed for discovery

This project combines genetic tool development with in vivo immunology to create and apply a contact-dependent cell-labeling system for studying autoimmune interactions. The approach moves from tool construction and validation to mechanistic application in a preclinical disease model.

Development of a novel cell-contact labeling tool enabling permanent genetic modification of neighboring cells, applied in a mouse model of psoriasis to map the interaction partners of skin-resident T cells.

Genetically engineered mouse models, skin-resident T cell populations in a psoriasis model, and contact-dependent labeling readouts to identify and characterize cellular interaction networks within the tissue microenvironment.

Characterization of the cellular and molecular factors that sustain skin-resident T cells in disease, with the goal of identifying targetable vulnerabilities that could be used to evict these cells from their niche and prevent psoriasis recurrence. The technology is also being evaluated for broader licensing potential across autoimmune disease research.

Investigators & Institutions

Powering the science

Principal Investigator

Susan R. Schwab, PhD, Colton Consortium Member

Professor, Department of Cell Biology; Department of Pathology, NYU Grossman School of Medicine, NYU Langone Health