---
title: "AA147 and Metabolically Activated Proteostasis Regulators Suppress CD4+ TH17 Differentiation"
id: "biorxiv-0-metabolically-activated-proteostasis-regulators-reduce-differentiation-of-cd4"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-0-metabolically-activated-proteostasis-regulators-reduce-differentiation-of-cd4"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.09.02.747634v1?rss=1"
published_at: "2026-09-05T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# AA147 and Metabolically Activated Proteostasis Regulators Suppress CD4+ TH17 Differentiation
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-0-metabolically-activated-proteostasis-regulators-reduce-differentiation-of-cd4
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.09.02.747634v1?rss=1)
- **Published At:** 2026-09-05T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The study reports that the metabolically activated proteostasis regulator **AA147** selectively reduces differentiation of pro-inflammatory **TH17** cells from naive CD4+ T cells. - AA147 was previously identified as a compound that can activate the ATF6 arm of the unfolded protein response (UPR) and, in some cell types, the **NRF2**-mediated oxidative stress response (OSR). - In this work, AA147 promotes degradation of the lineage-specifying transcription factor **RORgammat**, a key driver of TH17 identity, thereby reducing TH17 differentiation without altering transcription factors of other CD4+ T cell subsets. - The reduction of TH17 differentiation by AA147 is independent of **ATF6** activation and instead involves activation of **NRF2**, which lowers intracellular reactive oxygen species (**ROS**) levels to impede TH17 cell development. - AA147 also decreases expression of the TCR-responsive factor **IRF4**, which contributes to suppressed production of selected effector cytokines across effector T cell subsets, indicating broader dampening of effector cytokine responses. - The compound reshapes T cell subset activities via both **NRF2-dependent** and NRF2-independent mechanisms during differentiation. - The findings suggest pharmacologic targeting of stress-responsive pathways as a means to selectively remodel T cell subset differentiation, with AA147 as a candidate metabolically activated proteostasis regulator for modulating TH17 identity and effector responses. - The article is a preprint and has not been peer reviewed. A competing interest is declared: RLW is a shareholder and advisory board member of a company that has licensed proteostasis regulators including AA147; other authors report no conflicts.
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Priyadarshini Chatterjee 1 The Scripps Research Institute; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Priyadarshini%2BChatterjee%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Chatterjee%20P&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3APriyadarshini%2BChatterjee%2B) * [ORCID record for Priyadarshini Chatterjee](http://orcid.org/0009-0008-2002-8218 "Open in new tab") Keishla Sánchez Ortiz 1 The Scripps Research Institute; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Keishla%2BS%C3%A1nchez%2BOrtiz%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=S%C3%A1nchez%20Ortiz%20K&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AKeishla%2BS%25C3%25A1nchez%2BOrtiz%2B) * [ORCID record for Keishla Sánchez Ortiz](http://orcid.org/0000-0002-4537-3252 "Open in new tab") Stanislav Dikiy 1 The Scripps Research Institute; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Stanislav%2BDikiy%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Dikiy%20S&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AStanislav%2BDikiy%2B) * [ORCID record for Stanislav Dikiy](http://orcid.org/0000-0002-8287-6561 "Open in new tab") Michael J Bollong 1 The Scripps Research Institute; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Michael%2BJ%2BBollong%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Bollong%20MJ&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMichael%2BJ%2BBollong%2B) * [ORCID record for Michael J Bollong](http://orcid.org/0000-0001-9439-1476 "Open in new tab") Jessica E Thaxton 2 University of North Carolina at Chapel Hill; 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* [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Luke%2BWiseman%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Wiseman%20L&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ALuke%2BWiseman%2B) * [ORCID record for Luke Wiseman](http://orcid.org/0000-0001-9287-6840 "Open in new tab") * For correspondence: wiseman@scripps.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.09.02.747634v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5759608/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.09.02.747634v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5759608/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.09.02.747634v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5759608/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.09.02.747634v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5759608/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.09.02.747634v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5759608/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract The differentiation of naive CD4+ T cells into effector T cell subsets such as TH1, TH2, TH17 and TREG cells is governed by tightly coordinated activation programmes dependent on T cell receptor (TCR) engagement, co-stimulation, and cytokine signalling. This differentiation process involves regulation of stress-responsive signalling pathways such as the unfolded protein response (UPR) and the oxidative stress response (OSR) to adapt to the physiologic demands specific to distinct T cell subset functions. This suggests that pharmacologically targeting stress-responsive pathways offers a unique opportunity to selectively remodel the differentiation of these different T cell subsets. We previously identified compound AA147 as a metabolically activated proteostasis regulator that can induce both the ATF6 signalling arm of the UPR and, in certain cell types, the NRF2-regulated arm of the OSR. (Paxman et al., 2018; Plate et al., 2016) Here, we show that treatment with AA147 selectively reduces differentiation of pro-inflammatory TH17 cells by promoting degradation of the lineage-specifying transcription factor RORgammat, without impacting the transcription factors of other CD4+ T cell subsets. AA147-dependent reduction in TH17 differentiation is independent of ATF6 activation and involves activation of NRF2, which reduces intracellular reactive oxygen species (ROS) to hinder TH17 cell differentiation. Apart from RORgammat, we found that AA147 decreases expression of the TCR-responsive factor IRF4, thus suppressing production of select effector cytokines across effector T cells, demonstrating additional ways in which this compound reshapes the activities of these essential T cell subsets. Our results demonstrate the potential for metabolically activated proteostasis regulators such as AA147 to selectively reshape TH17 cell identity while broadly dampening effector cytokine responses across effector T cell subsets, through both NRF2-dependent and independent mechanisms during T cell differentiation. ### Competing Interest Statement RLW is a shareholder and scientific advisory board member of Protego Biopharma who has licensed proteostasis regulators including AA147 for commercial development. Other authors declare no conflicts. ## Funder Information Declared National Institutes of Health, AG046495, GM146865 Cancer Research Institute, https://ror.org/02f3xk561, Irvington Postdoctoral Fellowship Ellen Brown Scripps Foundation Prebys Foundation Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY 4.0 International license](http://creativecommons.org/licenses/by/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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[ Download PDF](https://www.biorxiv.org/content/10.64898/2026.09.02.747634v1.full.pdf) Print/Save Options [Download PDF](https://www.biorxiv.org/content/biorxiv/early/2026/09/05/2026.09.02.747634.full.pdf)Full Text & In-line FiguresXML [More Info](https://www.biorxiv.org/about/FAQ#PrintOptions "More Information on Print/Save Options") [Supplementary Material ](https://www.biorxiv.org/content/10.64898/2026.09.02.747634v1.supplementary-material) [ Email](https://www.biorxiv.org/ "Email this Article") [ Share](https://www.biorxiv.org/) Metabolically Activated Proteostasis Regulators Reduce Differentiation of CD4+ TH17 Cells Priyadarshini Chatterjee, Keishla Sánchez Ortiz, Stanislav Dikiy, Michael J Bollong, Jessica E Thaxton, Alejandra Mendoza, Luke Wiseman bioRxiv 2026.09.02.747634; doi: https://doi.org/10.64898/2026.09.02.747634 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. 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