Uncategorized Wednesday, 2024/10/16
More than 20 years ago, researchers at Yale University discovered a special type of T cell in the human body that can suppress the immune system. Later, they found that when defective, these so-called regulatory T cells can trigger some autoimmune diseases, especially multiple sclerosis (MS, multiple sclerosis). For many years, the molecular mechanisms behind this functional impairment have been unclear to researchers.
Recently, a research report titled "An autoimmune transcriptional circuit drives FOXP3+ regulatory T cell dysfunction" was published in the journal Science Translational Medicine. Scientists from Yale University School of Medicine and other institutions found that this lack of immune regulation may be caused by an increase in PRDM1-S protein, which often participates in multiple immune functions and can induce dynamic interactions between various genetic and environmental factors, including high salt intake; In the article, researchers also revealed a novel target for a universal therapy for treating human autoimmune diseases.
Our Related Proteins
| Cat.No. # | Product Name | Source (Host) | Species | Tag | Protein Length | Price |
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| FOXP3-51H | Recombinant Human Forkhead box P3, GST-tagged | Human | GST | 1-431 a.a. | ||
| SGK1-577H |
Active Recombinant Human SGK1, GST-tagged
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Sf9 Cells | Human | GST | 60-431 a.a. |
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| SGK1-3920H |
Active Recombinant Human SGK1 protein, His-tagged
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Insect Cells | Human | His |
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| SGK1-4993H |
Active Recombinant Human SGK1 protein, GST-tagged
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Insect Cells | Human | GST | M1-L431 |
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| Sgk1-145M | Recombinant Mouse Sgk1 protein, His-tagged | E.coli | Mouse | His | Ser145~Asp386 | |
| Prdm1-1928M | Recombinant Mouse Prdm1 protein, His & T7-tagged | E.coli | Mouse | His&T7 | Asn576~Val813 |
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| Prdm1-1929R | Recombinant Rat Prdm1 protein, His & T7-tagged | E.coli | Rat | His&T7 | Ser541~Lys815 |
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| PRDM1-1758H | Recombinant Human PRDM1 protein, His-tagged | E.coli | Human | His | Leu29~Asp149 |
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| FOXP3-59H | Recombinant Human FOXP3 protein, His-tagged | E.coli | Human | His | 230-431 aa | |
| FOXP3-60H | Recombinant Human FOXP3 protein, GST-tagged | E.coli | Human | GST | 107-196 aa | |
| FOXP3-1215H | Recombinant Human FOXP3 protein, His-tagged | E.coli | Human | His | Met1~Arg417 | |
| PRDM1-7062M | Recombinant Mouse PRDM1 Protein, His (Fc)-Avi-tagged | HEK293 | Mouse | Avi&Fc&His |
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Researcher Dr. Hafler said these experiments reveal the key mechanisms behind the loss of immune regulation in multiple sclerosis and other autoimmune diseases. At the same time, they also provide mechanistic insights into the molecular mechanisms behind the abnormal function of Treg cells (regulatory T cells) in human autoimmune diseases. Autoimmune diseases are one of the most common illnesses among young people, often influenced by genetic and environmental factors, including vitamin D deficiency and fatty acids. In an early study, researchers found that high levels of salt can also lead to the development of multiple sclerosis, which is an autoimmune disease of the central nervous system. Specifically, researchers observed that high salt can induce inflammation in an immune cell called CD4 T cells, while also causing the loss of regulatory T cell function, which may be mediated by the salt-sensitive kinase called SGK-1, which is critical for cell signaling.
In this latest study, researchers used RNA sequencing technology to compare gene expression differences between multiple sclerosis patients and healthy individuals. In multiple sclerosis patients, researchers identified upregulation or increased expression of the PRDM1-S (Primate Specific Transcription Factor, also known as BLIMP-1) gene, which is mainly involved in regulating immune function in the body. To the surprise of the researchers, they found that PRDM1-S can induce an increase in the expression level of salt-sensitive SGK-1 enzyme, leading to the destruction of regulatory T cells; In addition, they also found overexpression of PRDM1-S in patients with other autoimmune diseases, indicating that it may be a common feature of regulatory T cell dysfunction.
Researcher Sumida said that based on these research insights, they can now develop novel drugs to target and reduce the expression of PRDM1-S in regulatory T cells. They have already started collaborating with other researchers at Yale University to use novel computational methods to enhance the function of regulatory T cells, and to develop new methods applicable to the study of human autoimmune diseases. In summary, this study reveals a special mechanism model, in which the evolutionary emergence of PRDM1-S and the epigenetic initiation of AP-1/IRF (activator protein-1/interferon regulatory factor) may be key driving factors for the loss of Tregs cell function in autoimmune diseases.
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Reference
- Sumida TS, Lincoln MR, He L, Park Y, Ota M, Oguchi A, Son R, Yi A, Stillwell HA, Leissa GA, Fujio K, Murakawa Y, Kulminski AM, Epstein CB, Bernstein BE, Kellis M, Hafler DA. An autoimmune transcriptional circuit drives FOXP3+ regulatory T-cell dysfunction. Sci Transl Med. 2024 Aug 28;16(762):eadp1720. doi: 10.1126/scitranslmed.adp1720. Epub 2024 Aug 28. PMID: 39196959.