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FLT3LG — PTBP1

Text-mined interactions from Literome

Reber et al., Curr Drug Targets Immune Endocr Metabol Disord 2004 : This review focuses on the effects of Flt3L on DCs and other effector populations, and on its potential activity as a therapeutic agent for cancer, alone and in combination with vaccines
Shimizu et al., J Immunother 2004 (Neoplasms) : Because DC maturation stages affect their capacities of antigen processing and presentation, two DC populations were used for the current analysis : in vivo Flt-3 ligand induced mature DCs and in vitro bone marrow derived DCs, which were less mature
Toyama-Sorimachi et al., J Immunol 2005 : Freshly prepared murine plasmacytoid pre-DCs as well as Flt3L induced plasmacytoid pre-DCs expressed Ly49Q, whereas freshly prepared myeloid DCs did not
Morris et al., J Clin Invest 2005 (Leukemia, Experimental) : Enhanced cytotoxicity and GVL effects were not associated with Flt-3L signaling or effects on DCs but were reproduced by prolonged G-CSF receptor engagement with pegylated G-CSF
Curtin et al., J Immunol 2006 : Flt3L did not increase the numbers of conventional DCs , macrophages, or B, T, NK, NKT, or microglial cells within the brain
Zipris et al., J Immunol 2007 (Diabetes Mellitus, Type 1...) : Genomic KRV DNA also induces BBDR splenocytes and Flt-3L induced DCs from wild-type but not TLR9-deficient mice to produce IL-12p40 ; KRV induced up-regulation of B lymphocytes can be blocked by TLR9 antagonists including inhibitory CpG and chloroquine
Wolter et al., Clin Immunol 2009 (Diabetes Mellitus, Type 1) : Ex vivo and in vitro studies indicate that KRV upregulates proinflammatory cytokines and chemokines in B lymphocytes and Flt-3L induced plasmacytoid DCs ( pDCs )
Kingston et al., Blood 2009 : Combined lack of GM-CSF and Flt3-ligand in newly generated double-deficient mice leads to further significant reductions of DC progenitors and dermal DCs
Liu et al., J Immunol 2010 : CpG-B inhibition of IFN-alphabeta was observed in FLT3 ligand induced murine DCs , purified murine myeloid DCs, plasmacytoid DCs, and human PBMCs. CpG-B ODN inhibited induction of IFN-alphabeta by agonists of multiple receptors, including MyD88 dependent TLRs ( CpG-A ODN signaling via TLR9, or R837 or Sendai virus signaling via TLR7 ) and MyD88 independent receptors ( polyinosinic : polycytidylic acid signaling via TLR3 or ds break-DNA signaling via a cytosolic pathway )
Saito et al., Blood 2010 : Differentiation of bone marrow cells from SIRPa mutant mice into DCs induced by either macrophage-granulocyte colony stimulating factor or Flt3 ligand in vitro was not impaired
Bachem et al., Frontiers in immunology 2012 : Most importantly, we demonstrate that XCR1 ( + ) DCs in the spleen, LNs, and peripheral tissues are dependent on the growth factor Flt3 ligand and are selectively absent in Batf3-deficient animals
Siena et al., Exp Hematol 1995 (Neoplasms) : We show that the GM-CSF-plus-TNF-alpha dependent ex vivo generation of DCs from mobilized CD34+ cells is 2.5-fold enhanced by flk-2/flt-3 ligand or c-kit ligand ( stem cell factor ) and five-fold enhanced by a combination of these growth factors