FLT3 x Flt3L

Last update 08 May 2025

Basic Info

Related Targets

FLT3Flt3L

100 Clinical Results associated with FLT3 x Flt3L

100 Translational Medicine associated with FLT3 x Flt3L

0 Patents (Medical) associated with FLT3 x Flt3L

326

Literatures (Medical) associated with FLT3 x Flt3L

01 Dec 2025·Molecular Biology Reports

Effect of FLT3 ligand on the gene expression of TIM-3, HIF1-α, and TNF-α in an acute myeloid leukemia cell line

Article

Author: Gerdabi, Sajjad ; Kazemi-Sefat, Nazanin Atieh ; Ebtekar, Masoumeh ; Heidari, Fatemeh ; Pourfathollah, Ali Akbar ; Feizollahi, Parisa

BACKGROUNDAcute Myeloid Leukemia (AML) pathogenesis is driven by the dysregulation of various cell signaling pathways, including the FMS-Like Tyrosine Kinase 3 (FLT3) pathway and its ligand (FLT3L). These pathways play a critical role in promoting cell survival, proliferation, and resistance to apoptosis, contributing to leukemogenesis. In this study, we investigated the effects of FLT3L on the expression of key genes associated with immune regulation, hypoxia, and inflammation-TIM-3, HIF-1α, and TNF-α-in the THP-1 cell line, a well-established model for AML research.METHODSTHP-1 cells were cultured under standard conditions and treated with varying concentrations of FLT3L, alongside PMA as a positive control. Quantitative RT-PCR was employed to measure the expression levels of TIM-3, HIF-1α, and TNF-α genes after 48 h of treatment.RESULTSOur findings demonstrated that specific concentrations of FLT3L significantly upregulated the expression of TIM-3, HIF-1α, and TNF-α in THP-1 cells. This suggests that FLT3L not only influences cell proliferation and survival but also modulates pathways related to immune evasion, hypoxia adaptation, and inflammatory responses, which are hallmarks of leukemia progression.CONCLUSIONThese results highlight the pivotal role of FLT3L in regulating the expression of genes associated with AML pathogenesis, particularly those involved in hypoxia (HIF-1α), immune checkpoint regulation (TIM-3), and inflammation (TNF-α). The findings underscore the potential of targeting the FLT3 pathway as a therapeutic strategy in AML. Further studies are warranted to elucidate the underlying molecular mechanisms and explore their clinical implications for improving patient outcomes.

01 Jan 2025·International Journal of Medicinal Mushrooms

Dectin-1-Dependent Activation of Flt3 Ligand-Induced Dendritic Cells by the Caterpillar Medicinal Mushroom Cordyceps militaris (Ascomycetes) Fruiting Body

Article

Author: Nakasone, Toyokazu ; Tamura, Kazuhiro ; Okamatsu, Shigemi ; Miyaoka, Hiroaki ; Adachi, Yoshiyuki ; Tada, Rui ; Iwakura, Yoichiro ; Kanno, Takashi

Cordyceps militaris, an entomopathogenic fungus traditionally used in East Asian medicine, contains 1,3-β-glucans with well-known immunomodulatory properties. Our previous research has demonstrated that both fruit body powder and hot water extract of C. militaris can activate bone marrow-derived dendritic cells through dectin-1 signaling. However, the immunological effects on Fms-like tyrosine kinase 3 ligand-induced dendritic cells (fDCs), which closely resemble steady-state conventional dendritic cells in vivo, remain unexplored. In this study, we investigated the expression of dectin-1 in fDCs and its response to C. militaris fruit body powder (RK). Flow cytometric analysis revealed that conventional and plasmacytoid dendritic cells within the fDC population expressed dectin-1, with conventional dendritic cells showing particularly robust expression. Similar expression patterns were observed in freshly isolated splenic DCs. Importantly, RK induced significant tumor necrosis factor-α production in wild-type fDCs, whereas this effect was completely abolished in dectin-1-knockout fDCs. These findings demonstrate that C. militaris fruit-body powder activates fDCs through a dectin-1-dependent pathway, providing new insights into its immunomodulatory mechanisms and potential therapeutic applications.

23 Jul 2024·Journal of Virology

Flt3 agonist enhances immunogenicity of arenavirus vector-based simian immunodeficiency virus vaccine in macaques

Article

Author: Boopathy, Archana Vidya ; Sung, Janette ; Suthram, Silpa ; Geleziunas, Romas ; Wimmer, Raphaela ; Callebaut, Christian ; Nekkalapudi, Anurag ; Sharma, Bhawna ; Orlinger, Klaus K ; Schulha, Sophie ; Ng, Sarah ; Hung, Magdeleine ; Schmidt, Sarah ; Falkard, Brie ; Kuhne, Michelle ; Carr, Brian ; Jin, Debi ; Lauterbach, Henning ; Ahmadi-Erber, Sarah ; Lu, Sabrina

ABSTRACT Arenaviral vaccine vectors encoding simian immunodeficiency virus (SIV) immunogens are capable of inducing efficacious humoral and cellular immune responses in nonhuman primates. Several studies have evaluated the use of immune modulators to further enhance vaccine-induced T-cell responses. The hematopoietic growth factor Flt3L drives the expansion of various bone marrow progenitor populations, and administration of Flt3L was shown to promote expansion of dendritic cell populations in spleen and blood, which are targets of arenaviral vectors. Therefore, we evaluated the potential of Flt3 signaling to enhance the immunogenicity of arenaviral vaccines encoding SIV immunogens (SIV SME543 Gag, Env, and Pol) in rhesus macaques, with a rhesus-specific engineered Flt3L-Fc fusion protein. In healthy animals, administration of Flt3L-Fc led to a 10- to 100-fold increase in type 1 dendritic cells 7 days after dosing, with no antidrug antibody (ADA) generation after repeated dosing. We observed that administration of Flt3L-Fc fusion protein 7 days before arenaviral vaccine increased the frequency and activation of innate immune cells and enhanced T-cell activation with no treatment-related adverse events. Flt3L-Fc administration induced early innate immune activation, leading to a significant enhancement in magnitude, breadth, and polyfunctionality of vaccine-induced T-cell responses. The Flt3L-Fc enhancement in vaccine immunogenicity was comparable to a combination with αCTLA-4 and supports the use of safe and effective variants of Flt3L to augment therapeutic vaccine-induced T-cell responses. IMPORTANCE Induction of a robust human immunodeficiency virus (HIV)-specific CD4 + and CD8 + T-cell response through therapeutic vaccination is considered essential for HIV cure. Arenaviral vaccine vectors encoding simian immunodeficiency virus (SIV) immunogens have demonstrated strong immunogenicity and efficacy in nonhuman primates. Here, we demonstrate that the immunogenicity of arenaviral vectors encoding SIV immunogens can be enhanced by administration of Flt3L-Fc fusion protein 7 days before vaccination. Flt3L-Fc-mediated increase in dendritic cells led to robust improvements in vaccine-induced T- and B-cell responses compared with vaccine alone, and Flt3L-Fc dosing was not associated with any treatment-related adverse events. Importantly, immune modulation by either Flt3L-Fc or αCTLA-4 led to comparable enhancement in vaccine response. These results indicate that the addition of Flt3L-Fc fusion protein before vaccine administration can significantly enhance vaccine immunogenicity. Thus, safe and effective Flt3L variants could be utilized as part of a combination therapy for HIV cure.

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