# Role of Transcription Coactivator OCA-B in Gene Poising and Immunological Memory

> **NIH NIH R01** · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · 2020 · $495,529

## Abstract

PROJECT SUMMARY:
Immunological memory provides critical protection against pathogens and can drive autoimmune and anti-
tumor responses, but our understanding of the underlying molecular mechanisms is inadequate. The
transcriptional co-regulator OCA-B (also known as Bob.1, OBF-1 and Pou2af1) is induced in stimulated
primary CD4 T cells, where it docks with its cognate transcription factor Oct1 to regulate critical targets –
among them Il2, Il21, Ifng, Icos, Ctla4, Csf2 (Gmscf), Tnfrsf4 (Ox40), Tbx21 (Tbet), and Stat5a. OCA-B’s
effects do not manifest upon simple stimulation of CD4 T cells. Instead, withdrawing the stimulus, then
resting and re-stimulating OCA-B deficient cells results in gene expression defects of 100-fold or more.
OCA-B mediates these effects by recruiting the Jmjd1a histone lysine demethylase to remove inhibitory
histone H3K9me2 chromatin modifications at silent but previously activated target loci. In vivo, both OCA-B
and Oct1 are dispensable for T cell development and primary CD4 response but required for CD4 memory
formation and response to re-challenge1. This published foundational work leads to many unanswered
questions: Can OCA-B be used to prospectively identify CD4 memory cells? Can it directly drive memory?
What is its role in CD8 cells? In autoimmunity? In anti-tumor immunity? Why are OCA-B target genes
frequently adjacent to one another as linked gene pairs? Can OCA-B be targeted pharmacologically? Our
proposal addresses these questions. The overarching hypothesis is that in both CD4 and CD8 T cells,
OCA-B coordinately regulates the expression of genes encoding cytokines and other immunomodulatory
proteins to control pathogen response and memory cell formation. Aim 1: Determine if Jmjd1a recruitment
by myristoylated OCA-B promotes CD4 memory. Aim 2: Determine the role of OCA-B in chronic infection.
Aim 3: Determine if myristoylated OCA-B facilitates interactions between distant loci.

## Key facts

- **NIH application ID:** 9850503
- **Project number:** 5R01AI100873-07
- **Recipient organization:** UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH
- **Principal Investigator:** DEAN TANTIN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $495,529
- **Award type:** 5
- **Project period:** 2012-12-01 → 2022-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9850503

## Citation

> US National Institutes of Health, RePORTER application 9850503, Role of Transcription Coactivator OCA-B in Gene Poising and Immunological Memory (5R01AI100873-07). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9850503. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*