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LECT2 effect on the bone marrow cells of mice

ABSTRACT: Hematopoietic stem cell (HSC) is under dynamic controlled in the bone marrow to differentiate into cells of all lineages that constitute the blood. The bone marrow niches form a specific microenvironment to maintain and regulate HSC. However, the mechanisms that the effect of cytokines from blood on HSC function still remain largely unknown. Leukocyte chemotactic factor 2 (LECT2), a liver-derived cytokine, is involved in many immune dysfunctions, such as sepsis, cancer and diabetes. Here we showed that LECT2 affected the gene expression of bone marrow cells in mice. Especially, we found that LECT2 treatment for 3 and 5 days led to the down-regulation of cytokines such as, TNF, IL-6, IL-1β, CXCL10, CCL4, CCL3 et al. Moreover, the functions and mechanisms for LECT2 regulated HSC in bone marrow is still needed further investigation.

ORGANISM(S): Mus musculus

PROVIDER: GSE70014 | GEO | 2016/05/20

SECONDARY ACCESSION(S): PRJNA287488

REPOSITORIES: GEO

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Project description:We are studying the natural history, pathogenesis and treatment of patients with WHIM syndrome, an immunodeficiency disorder characterized by warts, hypogammaglobulinemia, recurrent infections and neutropenia usually due to autosomal dominant gain-of-function mutations in chemokine receptor CXCR4. We have identified a patient born with WHIM syndrome and the WHIM mutation CXCR4R334X who has been disease-free for 20 years and who lacks CXCR4R334X in myeloid cells, the cells that drive disease manifestations. She is a genetic and hematopoietic mosaic, since she still has the mutation in lymphoid cells and non-hematopoietic cells. Cytogenetics and microarray analysis revealed that the mechanism of loss of the mutation was deletion of the mutant allele from one copy of chromosome 2. Whole genome sequencing of patient neutrophil and skin fibroblast genomic DNA revealed that the mechanism of deletion was chromothripsis, a process of chromosome shattering resulting in deletions and rearrangements of the non-deleted chromosomal segments. In the patient, this process evidently occurred in a single hematopoietic stem cell (HSC), resulting in deletion of the disease allele CXCR4R334X and one copy of 163 other genes on chromosome 2. This HSC evidently acquired a growth advantage and repopulated the HSC population and the myeloid lineage. Consistent with this, studies using gene targeted mice in competitive bone marrow transplantation experiments revealed that selective Cxcr4 haploinsufficiency (inactivation of one copy of Cxcr4 and not of any other genes) was sufficient to confer a strong engraftment advantage over bone marrow cells from wild type mice as well as bone marrow cells from a mouse model of WHIM syndrome. These results suggest that CXCR4 knockdown may be a useful strategy to enhance bone marrow engraftment in the absence of toxic bone marrow conditioning regimens.

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LECT2 effect on the bone marrow cells of mice

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