Molecular Properties of a Factor Inducing Differentiation in Murine Myelomonocytic Leukemic Cells

Nicola, Nicos A.; Matsumoto, Miho; Metcalf, Donald; Johnson, Greg

doi:10.1007/978-3-642-68761-7_65

Cited by 23 publications

(27 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Bacterial products such as endotoxin, or inflammatory cytokines induced during infections, such as TNF, interleukin (IL-1) and IFNc, are the major stimulators of G-CSF production in vivo and result in a rapid but transient elevation in serum G-CSF levels. G-CSF is produced mainly by haematopoietic cells, such as monocytes/macrophages, and lymphocytes (Nicola et al, 1983;Sallerfors, 1994). Other cells, such as fibroblasts (Kaushansky et al, 1988), endothelial cells (Zsebo et al, 1988), astrocytes (Aloisi et al, 1992) and bone marrow stromal cells (Fibbe et al, 1988), can also produce G-CSF following activation by LPS, IL-1 or TNF-a.…”

Section: Discussionmentioning

confidence: 99%

Increased pathology in lungs of mice after infection with an α-crystallin mutant of Mycobacterium tuberculosis: changes in cathepsin proteases and certain cytokines

et al. 2006

View full text Add to dashboard Cite

Latency and reactivation are a significant problem that contributes to the incidence, transmission and pathogenesis of tuberculosis. The mechanisms involved in these processes, at the level of both the bacillus and the host, are poorly understood. In Mycobacterium tuberculosis the a-crystallin (acr) gene has been linked to latency, because it is highly expressed during hypoxic growth conditions. Deletion of the acr gene in M. tuberculosis H37Rv (Dacr strain) was previously shown to reduce the intracellular growth of bacilli in macrophages; however, its impact on pathogenesis in vivo was unknown. This study demonstrated that infection of C57BL6 mice with Dacr results in lung bacillary loads 1-2 log units higher in comparison to parental H37Rv. Haematoxylin/eosin staining of lungs revealed exacerbated pathology characterized by extensive obliteration of alveolar air spaces by granulomatous inflammation. RT-PCR analysis and immunostaining of lungs showed that infection with either H37Rv or Dacr results in the differential expression of lysosomal cathepsin proteases. A slight increase in the expression of the matrix-degrading acidic-type cathepsins B, D and H was noted in Dacr-infected mice and was associated with clusters of macrophages within lung granulomas. Dacr-infected mice also showed high serum levels of TNF-a, IFN-c and G-CSF, suggesting that Acr may play a role in modulating the host response to infection.

show abstract

Section: Discussionmentioning

confidence: 99%

Increased pathology in lungs of mice after infection with an α-crystallin mutant of Mycobacterium tuberculosis: changes in cathepsin proteases and certain cytokines

et al. 2006

View full text Add to dashboard Cite

show abstract

“…The other D-factor with a molecular mass of 20000-25 000 Da is produced by macrophages and has not yet been purified. G-CSF is also produced by macrophages [17] and the molecular mass of its glycosylated form is 25 000 Da [6]. Therefore, the D-factor for M I cells produced by macrophages might be identical to G-CSF.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, Nicola et al [6] reported that the differentiation factor for mouse myelomonocytic leukemic WEHI-3B cells is G-CSF, and Souza et al [7] showed that recombinant human G-CSF derived from bladder carcinoma 5637 cells induced differentiation of WEHI-3B cells and human leukemic cells. We also cloned a cDNA copy of the gene encoding human G-CSF from a cDNA library constructed from mRNA in macrophages [8].…”

Section: Introductionmentioning

confidence: 99%

Induction by recombinant human granulocyte colony‐stimulating factor of differentiation of mouse myeloid leukemic M1 cells

et al. 1986

View full text Add to dashboard Cite

The effect of recombinant human granulocyte colony‐stimulating factor (G‐CSF) on induction of differentiation of mouse myeloid leukemic M1 cells was examined. Purified G‐CSF caused dose‐dependent induction of phagocytic activity and lysozyme activity in M1 cells. Its half‐maximally effective concentration was 10 ng/ml. On treatment of M1 cells with G‐CSF (100 ng/ml) for 4 days, 30–50% of the cells differentiated morphologically into macrophage cells; 30–40% of the cells were blast cells and 20–30% of the cells were forms intermediate between blastic cells and mature macrophages.

show abstract

“…Hence activated macrophages in the synovium or possibly in the hematopoietic tissues are most likely responsible for the elevated systemic levels of IL-6 observed. IL-6 has been shown to be a potent inducer of macrophage and osteoclast differentiation (66,67). SOCS-3 is therefore important in the regulation of macrophage responses, and dysregulated synovial macrophage function may contribute to enhanced inflammatory arthritis.…”

Section: Figurementioning

confidence: 99%

SOCS-3 negatively regulates innate and adaptive immune mechanisms in acute IL-1-dependent inflammatory arthritis

Wong

Egan²,

Croker³

et al. 2006

Journal of Clinical Investigation

186

140

View full text Add to dashboard Cite

RA is an autoimmune disease characterized by sustained imbalance between pro-and antiinflammatory immune mechanisms. The SOCS proteins are negative regulators of cytokine signaling, but to date there has been little information on their function in disease. The generation of Socs3 -/Dvav mice, which lack SOCS-3 in the hematopoietic and endothelial cell compartment, allowed us to explore the role of endogenous SOCS-3 during acute inflammatory arthritis. Joint inflammation in Socs3 -/Dvav mice was particularly severe and was characterized by increased numbers of neutrophils in the inflamed synovium, bone marrow, peripheral blood, and spleen. These features were most likely due to increased production of and enhanced responsiveness to G-CSF and IL-6 during arthritis in these mice. Local osteoclast generation and bone destruction were also dramatically increased in the absence of SOCS-3, as was macrophage activation. Finally, SOCS-3 was found to negatively regulate CD4 + T lymphocyte activation, including production of the pleiotropic cytokine IL-17. The absence of SOCS-3 therefore had dramatic effects in this disease model, with a broader impact on cellular responses than SOCS-1 deficiency. These findings provide direct in vivo evidence that endogenous SOCS-3 is a critical negative regulator of multiple cell types orchestrating inflammatory joint disease.

show abstract

Molecular Properties of a Factor Inducing Differentiation in Murine Myelomonocytic Leukemic Cells

Cited by 23 publications

References 8 publications

Increased pathology in lungs of mice after infection with an α-crystallin mutant of Mycobacterium tuberculosis: changes in cathepsin proteases and certain cytokines

Increased pathology in lungs of mice after infection with an α-crystallin mutant of Mycobacterium tuberculosis: changes in cathepsin proteases and certain cytokines

Induction by recombinant human granulocyte colony‐stimulating factor of differentiation of mouse myeloid leukemic M1 cells

SOCS-3 negatively regulates innate and adaptive immune mechanisms in acute IL-1-dependent inflammatory arthritis

Contact Info

Product

Resources

About