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IL4 — STAT5A
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Friedrich et al., Int Immunol 1999
:
Activation of
STAT5 by
IL-4 relies on Janus kinase function but not on receptor tyrosine phosphorylation, and can contribute to both cell proliferation and gene regulation ... By functionally expressing receptor mutants in the murine pro-B cell line Ba/F3, we could show that phosphorylated tyrosine residues within the IL-4R alpha chain are dispensable for
IL-4 induced
STAT5 activity
Yamashita et al., J Exp Med 2000
:
Moreover, our results suggest that
IL-4 induced
STAT5 activation is required for the expansion process of developing Th2 cells
Mora et al., J Immunol 2001
:
However, transgenic cells exhibited a dramatic defect in Stat5A activation treatment with IL-2, and a similar defect was observed for
IL-4 induced
Stat5
Bream et al., Blood 2003
:
In exploring possible molecular mechanisms to account for the synergistic effects of IL-4 on murine NK cells, we found that IL-2 plus
IL-4 stimulation
resulted in a modest increase in tyrosine phosphorylation of
Stat5 , while IL-12 plus IL-4 treatment resulted in a more substantial increase in tyrosine phosphorylated Stat4
Zhu et al., Immunity 2003
:
Here, we report that retroviral ( RV ) -mediated expression of a constitutively active
Stat5A mutant ( STAT5A1*6 ) can fully
restore IL-4 production when naive CD4 T cells are primed in the absence of IL-2
Kay et al., Leuk Res 2005
(Leukemia, Lymphocytic, Chronic, B-Cell) :
Furthermore, when added to CLL B cells,
IL-4 induces increased apoptosis resistance, increased protein synthesis in CLL B cells and rapid onset activation of STAT1,
STAT5 and STAT6
Yagi et al., Int Immunol 2006
:
In addition,
IL-4 also
induced stronger
STAT5 activation in CD4 ( + ) T cells developing in BALB/c than in those developing in C57BL/6, whereas STAT6 was equally activated in these two cells ... Thus, our results indicate IL-2 induced
IL-4 production by naive CD4 ( + ) T cells, in which
STAT5 activation is
involved and directly controlled by the genetic background, to influence T ( h ) cell differentiation in murine strains
Stevenson et al., J Leukoc Biol 2009
:
We also discover that CCL11 inhibits GM-CSF mediated
STAT5 activation and
IL-4 induced STAT6
activation in a range of hematopoietic cells
Guo et al., Proc Natl Acad Sci U S A 2009
:
Th2 cells that have upregulated T1ST2 produce IL-13, but not
IL-4 , in
response to IL-33 plus a
STAT5 activator in an antigen independent, NF-kappaB dependent, cyclosporin A ( CsA ) -resistant manner
Murata et al., J Immunol 1996
(Colonic Neoplasms) :
Both IL-13 and
IL-4 induced phosphorylation of IL-4 STAT ( STAT6 ) but not STAT1, STAT3, or
STAT5
Hoefsloot et al., Blood 1997
(Myelodysplastic Syndromes) :
In contrast,
interleukin-3 induced a normal
STAT5 response in MDS cells
Moriggl et al., Mol Cell Biol 1997
:
Prolactin activates
Stat5 , and
interleukin-4 (IL-4) activates Stat6
Chida et al., Mol Endocrinol 1998
:
While
IL-4 does not
activate STAT5 , it induces expression of STAT5 regulated genes in CTLL-2, i.e. beta-casein, a cytokine-inducible SH2 containing protein ( CIS ), and oncostatin M (OSM), suggesting that STAT6 activated by IL-4 substitutes for the function of STAT5 in T cells
Ozaki et al., Blood 1998
:
Furthermore,
interleukin-3 (IL-3), granulocyte-macrophage colony stimulating factor ( GM-CSF ), and erythropoietin also
induce Crkl-STAT5 complex formation in responding cells in a stimulation dependent manner
Castro et al., J Immunol 1999
:
IL-4 selectively
inhibits IL-2 triggered
Stat5 activation, but not proliferation, in human T cells ...
IL-4 suppressed activation of DNA binding and tyrosine phosphorylation of the transcription factor
Stat5 by IL-2, and suppressed the expression of the IL-2-inducible genes CD25, CIS, the PGE2 receptor, and cytokine responsive ( CR ) genes CR1 and CR8