Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P13232 (
Interleukin-7
)
580
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Interleukin-7
(
IL-7
) is an important growth factor in B and T lymphopoiesis in mouse and human, whereas
IL-7
has been regarded to lack proliferative effects on cells within the myeloid lineage. However, we have recently reported that
IL-7
potently can enhance colony stimulating factor (CSF)-induced myelopoiesis from primitive murine hematopoietic progenitors, showing a novel role of
IL-7
in early murine myelopoiesis. Using CD34+ human hematopoietic progenitor cells, we show here a similar role of
IL-7
in human myelopoiesis, although interesting differences between the two species were found as well. Although purified recombinant human (rh)
IL-7
alone did not induce any proliferation of CD34+ cells,
IL-7
in a concentration-dependent manner enhanced the colony formation induced by all four CSFs up to threefold. Furthermore, stem cell factor (SCF)-induced granulocyte-macrophage (GM) colony formation was increased fourfold in the presence of
IL-7
. Single-cell cloning assays showed that these synergistic effects of
IL-7
were directly mediated on the targeted progenitors, and that
IL-7
increased the number, as well as the size of the colonies formed. Morphological examination showed that
IL-7
affected the progeny developed from CD34+ cells stimulated by
G-CSF
or IL-3, increasing the number of CFU-M (colony forming unit-macrophage) and CFU-granulocyte-macrophage, whereas the number of CFU-granulocyte were unaltered.
...
PMID:Direct synergistic effects of interleukin-7 on in vitro myelopoiesis of human CD34+ bone marrow progenitors. 751 74
Interleukin-7
(
IL-7
) stimulates the proliferation of normal and leukemic B and T cell precursors and T lymphocytes. Activation of the JAK/STAT pathway has been implicated in IL-7R signaling. We investigated which STAT complexes are formed upon stimulation of B cell precursor acute lymphoblastic leukemia (BCP-ALL) cells with
IL-7
. Gel retardation assays with STAT-binding oligonucleotides showed that
IL-7
induces the formation of two major STAT complexes in BCP-ALL cells. Supershifts with anti-STAT antibodies identified these as STAT1 and STAT5 complexes. This pattern of STAT activation was seen in all BCP-ALL cases that respond to
IL-7
in proliferation assays.
IL-7
also induced STAT/DNA binding in BCP-ALL cases that failed to proliferate in response to
IL-7
, suggesting that the ability of IL-7R to activate the JAK/STAT pathway per se is not sufficient for proliferation induction. To determine the contribution of the cytoplasmic domain of the
IL-7
receptor alpha chain (IL-7R alpha) to activation of STAT proteins, transfectants of the murine pro-B cell line BAF3 were made that express chimeric receptors consisting of the extracellular domain of human granulocyte colony-stimulating factor receptor (G-CSF-R) and the transmembrane and intracellular domains of human IL-7R alpha. Activation of the chimeric G-CSF-R/IL-7R alpha with
G-CSF
resulted in a full proliferative response and induced the phosphorylation of JAK1 but not JAK2. Major STAT complexes activated by G-CSF-R/IL-7R alpha contained STAT1 or STAT5, while some formation of STAT3-containing complexes was also seen. These findings establish that STAT1 and STAT5, and possibly STAT3, are activated upon stimulation of precursor B cells with
IL-7
. The data further indicate that the IL-7R alpha chains are directly involved in the activation of JAKs and STATs and have a major role in proliferative signaling in precursor B cells.
...
PMID:Interleukin-7 signaling in human B cell precursor acute lymphoblastic leukemia cells and murine BAF3 cells involves activation of STAT1 and STAT5 mediated via the interleukin-7 receptor alpha chain. 870 37
