Interleukin 3: Possible Roles in the Regulation of Lymphocyte Differentiation and Growth

Ihle, James N.; Rebar, L; Keller, JR; Lee, John C.; Hapel, Andrew J.

doi:10.1111/j.1600-065x.1982.tb00409.x

Cited by 151 publications

(41 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The data presented here show that cbl-b, but not ccbl, inhibits EGFR induced growth in 32D/EGFR cells ( Figure 5). These cells are absolutely dependent on growth factor (either EGF or IL-3) and rapidly undergo apoptosis in the absence of exogenous growth factor (Greenberger et al, 1983;Ihle et al, 1981Ihle et al, , 1982Pierce et al, 1988;Prystowsky et al, 1982). The inhibition of growth in the cbl-b clones is not associated with any cell cycle arrest but it is associated with a dramatic increase in the fraction of cells undergoing apoptosis (Figure 6).…”

Section: Discussionmentioning

confidence: 99%

“…The 32D cell line is a murine hematopoietic cell line which is absolutely dependent on exogenous IL-3 for sustained growth and it rapidly undergoes apoptosis in the absence of IL-3 (Greenberger et al, 1983;Ihle et al, 1981Ihle et al, , 1982Prystowsky et al, 1982). 32D cells do not normally express any endogenous EGFR (or other members of the EGFR family) and do not grow in EGF (Alimandi et al, 1997).…”

Section: E Ects Of Cbl-b and C-cbl On Egf Induced Cell Growth Of 32d/mentioning

confidence: 99%

See 1 more Smart Citation

cbl-b inhibits epidermal growth factor receptor signaling

et al. 1999

View full text Add to dashboard Cite

The role of cbl-b in signaling by the epidermal growth factor receptor (EGFR) was studied and compared with c-cbl. We demonstrate in vivo, that cbl-b, like c-cbl, is phosphorylated and recruited to the EGFR upon EGF stimulation and both cbl proteins can bind to the Grb2 adaptor protein. To investigate the functional role of cbl proteins in EGFR signaling, we transfected cbl-b or c-cbl into 32D cells overexpressing the EGFR (32D/EGFR). This cell line is absolutely dependent on exogenous IL-3 or EGF for sustained growth. 32D/EGFR cells overexpressing cbl-b showed markedly inhibited growth in EGF compared to c-cbl transfectants and vector controls. This growth inhibition by cbl-b was the result of a dramatic increase in the number of cells undergoing apoptosis. Consistent with this ®nding, cbl-b overexpression markedly decreased the amplitude and duration of AKT activation upon EGF stimulation compared to either vector controls or c-cbl overexpressing cells. In addition, the duration of EGF mediated MAP kinase and Jun kinase activation in cells overexpressing cbl-b is shortened. These data demonstrate that cbl-b inhibits EGF-induced cell growth and that cbl-b and c-cbl have distinct roles in EGF mediated signaling.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: E Ects Of Cbl-b and C-cbl On Egf Induced Cell Growth Of 32d/mentioning

confidence: 99%

cbl-b inhibits epidermal growth factor receptor signaling

et al. 1999

View full text Add to dashboard Cite

show abstract

“…This and other colonyinducing proteins were then renamed macrophage and granulocyte inducers (MGI) (Landau and Sachs, 1971) and MGI-type 1(MGI-1). They are now called colonystimulating factors (CSF) (reviewed in Metcalf, 1985;Sachs, 1987b) and one protein is called interleukin-3 (IL-3) (Ihle et al, 1982). Of these four CSFs, one (M-CSF), induces the development of clones with macrophages, another (G-CSF), clones with granulocytes, the third (GM-CSF), clones with granulocytes, macrophages, or both macrophages and granulocytes, and the fourth (IL-3), clones with macrophages, granulocytes, eosinophils, mast cells, erythroid cells, or megakaryocytes.…”

Section: Discovery Of Colony Stimulating Factorsmentioning

confidence: 99%

Cytokine control of developmental programs in normal hematopoiesis and leukemia

2002

View full text Add to dashboard Cite

“…IL-3 induces colony formation of multiple cell types in cultures of bone marrow or fetal liver cells . It supports the growth and/or differentiation of multipotent precursor cells belonging to both the myeloid and lymphoid lineages as well as more differentiated progenitor cells belonging to the myeloid lineage (2,(11)(12)(13)(14)(15). IL-3 has also been associated with multiple activities and has been termed burstpromoting activity (16), mast cell growth factor (17,18), P cell stimulating factor (19,20), and histamine-producing cell-stimulating factor (21) by various investigators.…”

mentioning

confidence: 99%

Activation and growth of colony-stimulating factor-dependent cell lines is cell cycle stage dependent.

London

McKearn

1987

The Journal of Experimental Medicine

View full text Add to dashboard Cite

Hematopoietic cell development is regulated by a series of growth factors that are progressively restricted in their biological activity. IL-3 is a multi-lineage growth factor that supports the growth and differentiation of progenitor cells belonging to multiple lineages. However, the mechanism by which IL-3 induces proliferation and differentiation of these cells is not completely understood. In this report, we have used two IL-3-dependent cell lines, FDC-P1 (a myeloid progenitor) and F15.12 (a lymphoid progenitor) to investigate IL-3-mediated growth and differentiation. When either FDC-P1 or FL5.12 cells are deprived of IL-3, greater than 90% of all cells accumulate in the G0 phase of the cell cycle. Upon readdition of IL-3, the cells will reenter the active phases of the cell cycle. Therefore, IL-3 can act as both a competence (G0----G1) factor, and a progression (G1----M) factor for hematopoietic precursor clones. FDC-P1 cells can also proliferate in response to granulocyte/macrophage colony-stimulating factor (G/M-CSF) and IL-4 (B cell stimulatory factor 1 [BSF-1]). However, resting (G0) FDC-P1 cells have lost their ability to grow in response to both G/M-CSF and IL-4, even though both factors can induce a G0----G1 transition. Therefore, G/M-CSF or IL-4 behave as progression factors among certain IL-3-responsive clones, and in those cases only in defined points in the cell cycle. Both IL-4 and G/M-CSF can maintain long-term growth of FDC-P1 cells. Upon removal of factor for 24 h, these clones accumulate in the G1 phase of the cell cycle and do not appear to enter G0 even after 36 h of factor deprivation. Therefore, cells maintained in G/M-CSF or IL-4 have altered growth requirements compared with the IL-3-dependent lines from which they were derived. The ability of various hematopoietic growth factors to regulate cell cycle progression in IL-3-dependent cell lines is dependent not only upon the lineage from which these cells were derived, but also the phase of the cell cycle in which those cells reside. The consequences of these interactions dictate the manner by which various clones will respond to CSFs and whether the cells will grow and/or differentiate.

show abstract

Interleukin 3: Possible Roles in the Regulation of Lymphocyte Differentiation and Growth

Cited by 151 publications

References 33 publications

cbl-b inhibits epidermal growth factor receptor signaling

cbl-b inhibits epidermal growth factor receptor signaling

Cytokine control of developmental programs in normal hematopoiesis and leukemia

Activation and growth of colony-stimulating factor-dependent cell lines is cell cycle stage dependent.

Contact Info

Product

Resources

About