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A study published in "Nature-Immunology", Blockade of IL-22 signaling reverses erythroid dysfunction in stress-induced anemias, showed that the immune signal transduction molecule interleukin-22 (IL-22) can inhibit the production of red blood cells and make mice suffer Upper anemia.
The research results may provide treatment ideas for stress-induced anemia in human patients.
Exposure to heavy metals such as radiation, pesticides, lead or mercury in the environment can increase the risk of myelodysplastic syndrome (MDS)-MDS is a collective term for a group of cancers, which is characterized by the inability of hematopoietic cells in the bone marrow to mature.
Often accompanied by severe anemia.
However, the mechanism leading to MDS is not yet fully clear.
Laurie Glimcher and colleagues at the Dana-Farber Cancer Institute in Boston, Massachusetts, USA, and colleagues identified a stress-induced feature that can lead to a decrease in red blood cells in mice with abnormal expression of Riok2-the human Riok2 gene is derived from chromosome 5.
This coding region is missing in 10%-15% of MDS patients.
The authors found that the decrease in Riok2 expression increases the expression of the immune signal transduction molecule IL-22.
The authors observed that the immature red blood cells of this mouse model are particularly sensitive to IL-22, and the increase in IL-22 levels will inhibit the development and maturation of red blood cells, and ultimately lead to cell death.
Subsequently, the authors proved that neutralizing IL-22 with antibody therapy can restore red blood cell production.
The authors also observed increased levels of IL-22 in a cohort of human patients with MDS with mutations in chromosome 5 and another cohort of human patients with anemia and chronic kidney disease, indicating that IL-22 may be used as one of these diseases.
Biomarkers.The author believes that although further research is still needed, combining the above results shows that targeting the IL-22 signal transduction pathway may help reduce stress-induced anemia in human patients.
The decrease in Riok2 gene expression leads to an increase in p53, which in turn drives the increase in IL-22 expression.
Picture from Glimcher et al.
©Nature Nat Immu | doi: 10.
1038/s41590-021-00895-4
The research results may provide treatment ideas for stress-induced anemia in human patients.
Exposure to heavy metals such as radiation, pesticides, lead or mercury in the environment can increase the risk of myelodysplastic syndrome (MDS)-MDS is a collective term for a group of cancers, which is characterized by the inability of hematopoietic cells in the bone marrow to mature.
Often accompanied by severe anemia.
However, the mechanism leading to MDS is not yet fully clear.
Laurie Glimcher and colleagues at the Dana-Farber Cancer Institute in Boston, Massachusetts, USA, and colleagues identified a stress-induced feature that can lead to a decrease in red blood cells in mice with abnormal expression of Riok2-the human Riok2 gene is derived from chromosome 5.
This coding region is missing in 10%-15% of MDS patients.
The authors found that the decrease in Riok2 expression increases the expression of the immune signal transduction molecule IL-22.
The authors observed that the immature red blood cells of this mouse model are particularly sensitive to IL-22, and the increase in IL-22 levels will inhibit the development and maturation of red blood cells, and ultimately lead to cell death.
Subsequently, the authors proved that neutralizing IL-22 with antibody therapy can restore red blood cell production.
The authors also observed increased levels of IL-22 in a cohort of human patients with MDS with mutations in chromosome 5 and another cohort of human patients with anemia and chronic kidney disease, indicating that IL-22 may be used as one of these diseases.
Biomarkers.The author believes that although further research is still needed, combining the above results shows that targeting the IL-22 signal transduction pathway may help reduce stress-induced anemia in human patients.
The decrease in Riok2 gene expression leads to an increase in p53, which in turn drives the increase in IL-22 expression.
Picture from Glimcher et al.
©Nature Nat Immu | doi: 10.
1038/s41590-021-00895-4
