[ad_1]
Inflammatory and autoimmune diseases such as psoriasis, rheumatoid arthritis and multiple sclerosis (MS) are a major health burden worldwide and constitute a life-threatening condition for afflicted patients. Yet, if one knows a lot about the mechanisms of the disease, there are in most cases very few effective therapeutic options.
However, a recent study published in Nature Communications gives hope to people suffering from autoimmune diseases. Under the guidance of researchers from Osaka University, the research team discovered that the genomic host protein Satb1 induces a change in immune cells, inducing tissue inflammation and autoimmunity . This breakthrough could lead to new treatments targeting the source of inflammation.
Interleukin 17-producing helper (Th17) helper cells are a clbad of newly identified immune cells that play a major role in protecting against the invasion of pathogens. But despite their name, Th17 cells are not always so useful. In fact, studies have shown that excessive Th17 cell-mediated inflammation is actually one of the underlying causes of many inflammatory and autoimmune disorders.
But what makes Th17 cells cross the line from useful to harmful?
To answer this question, the researchers examined the organizing protein of the Satb1 genome. "We have known for some time that Satb1 is essential for the development of T cells in the thymus, but its involvement in the regulation of pathogenic processes of Th17 cells in inflamed tissues has not been examined," explains Dr. Principal author Keiko. Yasuda.
Using a mouse model of SP, the researchers deleted the Satb1 gene in Th17 cells and found that the disease no longer developed in mutant mice. The key to this mechanism was the lack of expression of a protein called granulocyte-macrophage colony stimulating factor (GM-CSF) by defective Th17 cells. GM-CSF is a pathogenic cytokine that causes tissue inflammation localized in MS and other inflammatory autoimmune diseases. Importantly, Satb1 has also been shown to enhance GM-CSF gene expression, thus confirming its role in promoting inflammation in sick individuals.
Satb1 seems to not only promote inflammation, but also block the expression of a protein specifically designed to suppress the inflammatory activity of T cells and prevent autoimmune diseases. This protein, the programmed cell death protein 1, was more strongly expressed in Satb1 deficient Th17 cells than normal Th17 cells, indicating that Satb1 normally inhibits the expression of the protein.
As the author corresponding to the study, Shimon Sakaguchi, explains, these findings are interesting: "Our results suggest that manipulation of Satb1 gene expression in Th17 cells could constitute the Based on new treatments for various autoimmune diseases caused by Th17 cells, if we can prevent pathogenic processes of Th17 cells, we may be able to mitigate or even eliminate the symptoms of the disease. "
Source of the story:
Material provided by University of Osaka. Note: Content can be changed for style and length.
Source link
