Postdoctoral Fellow, Genetic Mechanisms & Target Discovery in Autoimmune Disease

The Team

Our immune cell reprogramming team integrates foundational research on immunology and disease biology with AI-modeling to develop engineered cells that harness our own immune system to detect and treat early signs of age-related diseases, like cancer, Alzheimer’s, and Parkinson’s. These technologies will enable precise, context-dependent therapeutic responses only when and where it is needed. You can learn more about our work here. 

Our work brings together three powerhouse universities - Columbia University, The Rockefeller University, and Yale University - into a single collaborative technology and discovery engine.

Our Vision

• Pursue large scientific challenges that cannot be pursued in conventional environments
• Enable individual investigators to pursue their riskiest and most innovative ideas
• Facilitate research by scientists and clinicians at our home institutions and beyond

We are a team of passionate individuals powered by technology, guided by scientific research, and driven by collaboration, working toward a mission to cure or prevent all disease.

The Opportunity

The Laboratory of Immunogenomics at Biohub in NY (www.mahatlab.com) studies the non-coding regulatory genome to understand and address immune dysfunction in diseases like cancer, autoimmune disorders, and aging. We focus on enhancers—non-coding, highly cell-type-specific transcriptional regulatory elements—and their role in shaping immune responses.

We develop and utilize genomic technologies, including bulk and single-cell nascent RNA sequencing, genome editing, immune engineering, and CRISPR-based functional screens in patient biopsies, organoid systems, and mouse models. Through computational analysis integrating machine learning and AI, we map enhancer–gene networks and identify disease-driving elements. Our goal is to advance enhancer-guided precision genomic medicine for diseases involving immune dysfunction.

We seek a Postdoctoral Fellow to dissect the non-coding genomic mechanisms underlying common autoimmune diseases (e.g., Type 1 Diabetes, Systemic Lupus Erythematosus, Celiac Disease, etc.). Over 80% of autoimmune disease-associated variants map to non-coding regions across numerous susceptibility loci, yet their target genes, relevant cell types, and molecular mechanisms remain largely unknown. This project aims to identify causal regulatory variants, map their cell-type-specific effects, and link genetic variation to immune dysfunction and disease phenotypes.

What You'll Do

• Variant Prioritization and Fine-Mapping
• Apply Bayesian fine-mapping (FINEMAP, SuSiE) to GWAS loci, integrating multi-ancestry data.
• Overlay variants with nascent RNA sequencing, open chromatin regions, histone modifications, and transcription factor motifs across relevant immune and target cell types. 
• Cell-Type-Specific Mechanism Mapping
• Perform single-cell eQTL analysis in disease-relevant cell types (e.g., T cell subsets, B cell subsets, monocytes, or target-tissue cells) from patients.
• Map stimulus-dependent effects under key inflammatory or activating conditions (e.g., IFN, TLR agonists, TCR/BCR stimulation).
• Use promoter-capture Hi-C or similar methods to identify variant target genes through long-range chromatin interactions.
• Functional Validation
• Execute MPRAs (Massively Parallel Reporter Assays) testing allele-specific enhancer activity for prioritized variants.
• Deploy CRISPR base editing to introduce risk alleles into relevant cell lines and primary cells.
• Run CRISPRi/a screens targeting regulatory elements, measuring effects on core disease-driving pathways.
• Pathway Integration and Target Identification
• Map variant-regulated genes to core disease pathways.
• Build regulatory networks connecting variants to key disease-associated transcription factors and downstream immune programs.
• Identify druggable targets within variant-affected pathways for therapeutic development.
• Patient-Derived Studies
• Isolate and functionally test primary immune or target cells from patients carrying specific risk haplotypes.
• Develop polygenic risk scores stratifying patients by pathway involvement.
• Correlate variant effects with clinical subtypes (e.g., disease-specific organ involvement or systemic manifestations).

What You'll Bring

Essential 

• PhD in Genetics or Genomics with a dissertation focused on autoimmune or inflammatory diseases.
• Direct experience in systemic or organ-specific autoimmune diseases (e.g., SLE, T1D, systemic sclerosis), or related B/T cell-mediated disorders.
• Hands-on expertise with at least two: eQTL mapping, nascent RNA sequencing, MPRA/reporter assays, CRISPR editing in primary cells.
• Proficiency in isolating and culturing primary human B cells, T cells, or myeloid/target-tissue cells.
• Publication record demonstrating variant-to-function work or autoimmune disease mechanisms.

Preferred

• Experience with GWAS fine-mapping tools and integrating genetic with epigenomic datasets.
• Single-cell multiomics: scRNA-seq, scATAC-seq, or CITE-seq with analysis pipelines.
• CRISPR-based editing or prime editing in hard-to-transfect primary immune cells.
• Knowledge of core immune cell biology (e.g., T/B cell activation, germinal center reactions, autoantibody production) and key signaling pathways (e.g., type I interferon biology, JAK-STAT signaling).

Compensation

The New York, NY base pay for a new hire in this role is Postdoctoral Fellow = $93,000.00

Benefits for the Whole You 

We’re thankful to have an incredible team behind our work. To honor their commitment, we offer a wide range of benefits to support the people who make all we do possible. 

• Provides a generous employer match on employee 401(k) contributions to support planning for the future.
• Paid time off to volunteer at an organization of your choice. 
• Funding for select family-forming benefits. 
• Relocation support for employees who need assistance moving

If you’re interested in a role but your previous experience doesn’t perfectly align with each qualification in the job description, we still encourage you to apply as you may be the perfect fit for this or another role.

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