Aberrant overexpression of CD14 on granulocytes sensitizes the innate immune response in mDia1 heterozygous del(5q) MDS
Aberrant overexpression of CD14 on granulocytes sensitizes the innate immune response in mDia1 heterozygous del(5q) MDS
Key PointsmDia1 deficiency led to a cell-autonomous overexpression of CD14 on granulocytes and a hypersensitive innate immune response. mDia1 heterozygous and knockout mice developed age-dependent MDS that was accelerated by chronic stimulation of the innate immunity.
- University of Oxford United Kingdom
- Boston Children's Hospital United States
- Albert Einstein College of Medicine United States
- Dana-Farber Cancer Institute United States
- Moffitt Cancer Center United States
Lipopolysaccharides, Male, Mice, Knockout, Heterozygote, Lipopolysaccharide Receptors, Formins, Bone Marrow Cells, Immunity, Innate, Mice, Gene Expression Regulation, Myelodysplastic Syndromes, Animals, Chromosomes, Human, Pair 5, Humans, Female, RNA, Messenger, Chromosome Deletion, Carrier Proteins, Adaptor Proteins, Signal Transducing, Granulocytes
Lipopolysaccharides, Male, Mice, Knockout, Heterozygote, Lipopolysaccharide Receptors, Formins, Bone Marrow Cells, Immunity, Innate, Mice, Gene Expression Regulation, Myelodysplastic Syndromes, Animals, Chromosomes, Human, Pair 5, Humans, Female, RNA, Messenger, Chromosome Deletion, Carrier Proteins, Adaptor Proteins, Signal Transducing, Granulocytes
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