Scientists found incentives for inflammatory anemia

Scientists found incentives for inflammatory anemia

January 30, 2019 Source: Ministry of Science and Technology

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Recently, researchers at the University of Washington and the Benaroya Institute published an article entitled "Chronic TLR7 and TLR9 signaling drives anemia via differentiation of specialized hemophagocytes" in Science. They identified monocyte differentiation pathways associated with inflammatory cytopenia and caused by Toll-like receptors 7 and 9, and found that iHPCs (inflammatory hemophagocytic cells) are the cause of inflammatory anemia for the treatment of macrophages. Activation syndrome, severe malaria anemia, and inflammatory anemia provide theoretical support.

Anemia and thrombocytopenia are associated with infectious and autoimmune diseases, and severe inflammatory cytopenia, called macrophage activation syndrome, occurs during rheumatism and viral infections. In mice, the researchers found that monocyte recognition by self- or pathogen-derived nucleic acids caused by Toll-like receptors 7 and 9 (TLR7 and TLR9) induces macrophage activation syndrome-like disease. Monocytes differentiate into iHPCs by TLR7 or TLR9 signaling, and macrophage activation syndrome-like symptoms can be alleviated by means of removing monocytes to prevent differentiation of iHPCs. In addition, the researchers also found differentiation of MyD88 (myeloid differentiation factor 88)- and endosomal TLR-dependent iHPCs in a mouse malaria anemia model. Therefore, iHPCs are a major cause of macrophage activation syndrome, malaria anemia, and thrombocytopenia.

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