The Role of a Key Transcription Factor PU.1 in Autoimmune Diseases
Open accessAbstract
PU.1, a transcription factor member of the E26 transformation-specific family, affects the function of a variety of immune cells in several physiological and pathological conditions. Previous studies studying the role of PU.1 in pathological conditions have mainly focused on immune system-related cancers, and a series of articles have confirmed that PU.1 mutation can induce a variety of immune cell-related malignancies. The underlying mechanism has also been extensively validated. However, the role of PU.1 in other major immune system-related diseases, namely, systemic autoimmune diseases, is still unclear. It was only in recent years that researchers began to gradually realize that PU.1 also played an important role in a variety of autoimmune diseases, such as rheumatoid arthritis (RA), experimental autoimmune encephalomyelitis (EAE) and systemic lupus erythematosus (SLE). This review article summarizes the findings of recent studies that investigated the role of PU.1 in various autoimmune diseases and the related underlying mechanisms. Furthermore, it presents new ideas and provides insight into the role of PU.1 as a potential treatment target for autoimmune diseases and highlights existing research problems and future research directions in related fields.
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PU.1 functions as an immune activator by inducing the expression of IL-9 and CD80.
“PU.1 also functions as an immune activator by inducing the expression of IL‐9 and CD80 [58, 59, 60].”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [60]
The ‘PU.1 in rheumatoid arthritis’ section (page unavailable) says PU.1 binds the IL-9 promoter and is essential for Th9-related inflammation, supporting the IL-9 and immune-activation part of the claim. Our copy does not report PU.1 inducing CD80 expression (searched: CD80 and PU.1 expression). (LLM, conf=0.84)
Experimental — accuracy not yet measuredPathogenic myeloid cell activity in the context of autoimmunity and chronic inflammatory disease has been attributed to PU.1-dependent gene programs.
“Of note, pathogenic myeloid cell activity in the context of autoimmunity and chronic inflammatory disease has been attributed to PU.1-dependent gene programs (Fang et al., 2022)”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as Fang et al., 2022
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Cited by
Sorted by citations
PU.1 is required to restrain myelopoiesis during chronic inflammatory stress
Chavez, J. S., Rabe, J. L., Niño, K. E., Wells, H. H., Gessner, R. L., Mills, T. S., Hernandez, G., & Pietras, E. M. (2023) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1204160 · Cited by 14 · see citing works
“1-dependent gene programs (Fang et al., 2022), raising the question as to whether PU.”
BackgroundTargeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease
Kim, B., Wang, S. S., Kim, J. R., & Kim, J. (2026) · BioEssays · doi:10.1002/bies.70186
“PU.1 also functions as an immune activator by inducing the expression of IL-9 and CD80 [58–60].”
- Authors
- Fang, Y., Chen, W., Li, Z., Chen, Y., Wu, X., Zhu, X., Wang, H., Chen, X., Liang, Q., Huang, J., Han, X., Hong, W., Wang, X., Wei, W., Yu, Z., & Tu, J.
- Affiliations
- Anhui Medical University (CN)
- Southern Medical University (CN)
- Shenzhen University Health Science Center (CN)
- First Affiliated Hospital of Anhui Medical University (CN)
- Corresponding author
- Wei, Wei
- Yu, Zhiying
- Tu, Jiajie
- ORCID
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2022-09-29
- Volume
- 13
- Pages
- 1001201-1001201
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC9557192
- OpenAlex
- W4303184314
- Cited by
- 31
- References
- 9
- Citations by year
- 2026: 10 · 2025: 11 · 2024: 5 · 2023: 5
- FWCI
- 0.87
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Anhui Medical University (2020xkjT009)
- Shenzhen Municipal Science and Technology Innovation Council (JCYJ20210324102806018, JCYJ20210324103001003)
- Sanming Project of Medicine in Shenzhen (JCYJ20210324102806018, SZSM201812041)
- Topics
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Keywords
- PU.1, ETS transcription factors, autoimmune disease, rheumatoid arthritis, experimental autoimmune encephalomyelitis, systemic lupus erythematosus, immune cell function, therapeutic target
- MeSH terms
- Proto-Oncogene Protein Spi-1, Animals, Encephalomyelitis, Autoimmune, Experimental, Lupus Erythematosus, Systemic, Neoplasms, Proto-Oncogene Proteins, Transcription Factors, Trans-Activators
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