CLEC4C _ BDCA2
- Known as:
- CLEC4C _ BDCA2
- Catalog number:
- Y214307
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CLEC4C _ BDCA2
Related genes to: CLEC4C _ BDCA2
- Gene:
- CLEC4C NIH gene
- Name:
- C-type lectin domain family 4 member C
- Previous symbol:
- CLECSF11, CLECSF7
- Synonyms:
- HECL, DLEC, BDCA2, CD303
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-12-21
- Date modifiied:
- 2016-10-05
Related products to: CLEC4C _ BDCA2
Antibodies: CLEC4C _ BDCA2 HOST: Goat Clonality: pAbBDCA2,BDCA-2,Blood dendritic cell antigen 2,CLEC4C,CLECSF11,CLECSF7,C-type lectin domain family 4 member C,C-type lectin superfamily member 7,Dendritic lectin,DLEC,HECL,Homo sapiens,Human,UNQ9361_PRO3Bovine C-type lectin domain family 4 member C(CLEC4C) ELISA kitCanine C-type lectin domain family 4 member C(CLEC4C) ELISA kitCanine C-type lectin domain family 4 member C(CLEC4C) ELISA kitChicken C-type lectin domain family 4 member C(CLEC4C) ELISA kitCLEC3B Gene C-type lectin domain family 3, member BCLEC4CCLEC4C 3&_39;UTR Lenti-reporter-Luc VectorCLEC4C AntibodyCLEC4C antibodyCLEC4C AntibodyCLEC4C antibody Polyclonal Antibodies Primary antibodiesCLEC4C antibody Polyclonal Antibody Host: GoatCLEC4C Antibody. Related articles to: CLEC4C _ BDCA2
- Vidutolimod (Vidu) is a nanosized virus-like particle (VLP) composed of the Qβ bacteriophage capsid assembled around a Toll-like receptor 9 (TLR9) agonist. immunization with Vidu through intratumoral injection can induce a systemic anti-tumor immune response and has shown promise in early phase cancer clinical trials. Activation of intratumoral plasmacytoid dendritic cells (pDCs), and their production of type I interferon (IFN), plays a key role in initiating the anti-tumor response to Vidu and is dependent on coating of the VLP by antibodies against the Qβ capsid (anti-Qβ). Here we evaluated the mechanisms responsible for the binding, internalization and response of pDCs to anti-Qb-coated Vidu. - Source: PubMed
Publication date: 2026/02/12
Lemke-Miltner Caitlin DBlackwell Sue EYin ChaoboFischer Travis DWeiner George J - Triple-negative breast cancer (TNBC) represents the most aggressive breast cancer subtype, with its highly heterogeneous tumor microenvironment posing substantial challenges for precision diagnosis and therapy. To address this, we aim to construct a novel prognostic framework based on tumor-immune interactions. Through integrative analysis of single-cell RNA sequencing data from 30 TNBC samples (106,132 cells), we identify key tumor expression metaprograms and uncover their interaction with an immunosuppressive dendritic-cell subset, a process associated with the NECTIN1-NECTIN4 axis. Leveraging these interactions, we developed and validated two immunological prognostic models using multi-cohort transcriptomic data, including the stress response tumor cell and pDC_CLEC4C prognostic model (SPSM) and the immune response tumor cell and pDC_CLEC4C prognostic model (IPSM). These models effectively stratified TNBC patients into distinct risk groups, with the low-risk group characterized by an immunologically active microenvironment and elevated expression of immune checkpoint genes, suggesting a potential responsiveness to immunotherapy. Furthermore, we identified several potential therapeutic agents, including imatinib and bortezomib. Collectively, our dual-model framework provides a tool for risk stratification, offers translational insights for precision treatment, and presents new directions for understanding TNBC heterogeneity and therapeutic development. - Source: PubMed
Publication date: 2026/02/03
Lin ShihuaWang HongjiuWang ZhenzhenXiao YuxuanPatrice Menoudji DjetoyomWang LiLi XiaZhang Yunpeng - Acute graft-versus-host disease (GVHD) of the gastrointestinal tract is a primary cause of early transplant mortality after bone marrow transplantation (BMT), driven by local antigen presentation and T-cell expansion. We sought to clarify the role of various subsets of donor dendritic cells (DC) in this process to define therapeutic strategies to prevent gut GVHD. Donor plasmacytoid DC (pDC) were prominent in the ileum of BMT recipients without GVHD but were largely absent in gut during GVHD. In contrast, donor XCR1+ conventional DC (cDC) were dramatically increased in the mesenteric lymph nodes of BMT recipients with GVHD. We utilized Xcr1-DTR mice and Clec4c-DTR mice to enable highly efficient XCR1+ cDC vs pDC depletion. Donor XCR1+ cDC but not pDC deletion attenuated lethal GVHD, depleting most cDC presenting alloantigen, which inhibited α4β7 and the expansion of alloantigen-specific donor Th1 cells in the gut. Aldehyde dehydrogenase 1A (ALDH1A) expression by cDC is known to modulate GVHD and we thus examined the effect of a pan-ALDH1 inhibitor, WIN18446, on this axis. WIN18446 administration improved survival and these effects were ALDH1A1-specific but mediated by inhibition of CD11b+ rather than XCR1+ cDC, inhibiting alloantigen-specific Th17 cell differentiation in the gut. These findings highlight the limited role of pDC in the induction of gut GVHD and identify differential and dominant roles for XCR1+ and CD11b+ donor cDC in controlling Th1- and Th17-mediated gut aGVHD. The targeting of donor cDC subsets represents an effective strategy to prevent lethal gut GVHD. - Source: PubMed
Takahashi ShuichiroInoue TakayukiEnsbey Kathleen SLegg Samuel R WSekiguchi TomokoNelson EthanNemychenkov Nicole SJoshi TanviMinnie Simone AYeh Albert CZhang PingHeadley MarkPaik JisunAmory John KHill Geoffrey RKoyama Motoko - The prognostic role of dendritic cells (DCs) in colorectal cancer (CRC) and paired liver metastases (LM) remains unclear, particularly regarding the dynamics of immature CD1a and mature CD208 subsets across anatomical compartments and synchronous versus metachronous disease. - Source: PubMed
Publication date: 2025/12/18
Pavlov SergiiAli EsraaYe WenjingČervenková LenkaAmbrozkiewicz FilipVyčítal OndřejDaum OndřejLiška VáclavHemminki KariTrailin Andriy - Plasmacytoid dendritic cells (pDCs) are a unique subset of dendritic cells specialized in rapid and robust type I interferon (IFN) production, playing critical roles in the pathogenesis and pathomechanisms of many human diseases. Accurate identification of pDCs in peripheral blood mononuclear cells (PBMCs) is challenging due to dynamic and non-exclusive specific expression of surface markers such as blood dendritic cell antigen (BDCA)-2 and BDCA-4. Although BDCA-4 is generally more stably expressed than BDCA-2, prolonged stimulation or inflammatory conditions can induce its expression on multiple non-pDC cell types, reducing the accuracy of pDC identification. Here, we thoroughly investigated BDCA-4 expression dynamics on pDCs and other PBMC subsets following prolonged activation with Toll-like receptor (TLR) 7 and TLR9 agonists. Our flow cytometry analysis revealed a significant increase in BDCA-4-positive non-pDC populations after extended stimulation, primarily corresponding to CD14 monocytes. To overcome this limitation, we performed a gating strategy combining BDCA-4 positivity with a cocktail of non-pDC markers, enabling the exclusion of non-pDCs and accurate identification of pDCs. This approach enables the reliable identification of pDCs within heterogeneous cell populations using only two fluorescent channels in healthy conditions and even during strong activation or pathological states characterized by chronic inflammation. - Source: PubMed
Publication date: 2025/11/13
Demeter SaroltaFekete TündeScholtz BeátaVeréb ZoltánKemény LajosBácsi AttilaPázmándi Kitti