Details for: CL0001058

Cell ID: CL0001058

Cell Name: plasmacytoid dendritic cell, human

Description: This cell type is compatible with the HIPC Lyoplate markers for 'plasmacytoid dendritic cell'. The inclusion of HLA-DRA in the definition restricts this definition to human plasmacytoid dendritic cells.

Synonyms: plasmacytoid dendritic cell

Selected Context(s): Overall

Gene Significance Landscape

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Score:
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Genes

Contexts:

Cell Significance Index (CSI) is uniquely calculated to reveal cell-specific gene markers. More info here

Significant Genes List

Genes with the highest and lowest Percentile Rank Scores (PRS) for plasmacytoid dendritic cell, human within the selected context(s).

Gene ID: A unique numerical identifier for this specific gene.
Symbol: Shortened abbreviation or name that represents this gene.
Ensembl Gene ID: A unique identifier assigned by Ensembl for genomic data mapping.
CSI Score: A combined effect size and statistical significance measure for plasmacytoid dendritic cell, human. Higher scores indicate a stronger, more significant difference in expression.
(Previously described as "Fold Change", but now represents Cliff's Delta × –log10(p).)

Gene ID: A unique numerical identifier for this specific gene.
Symbol: Shortened abbreviation or name that represents this gene.
Ensembl Gene ID: A unique identifier assigned by Ensembl for genomic data mapping.
CSI Score: A combined effect size and statistical significance measure for plasmacytoid dendritic cell, human. Higher scores indicate a stronger, more significant difference in expression.
Average CSI: csi sum / gene count
Cell network configuration

This network visualizes key genes for plasmacytoid dendritic cell, human. It primarily includes:
1. Top genes highly significant for this cell (Num. Top Cell Genes - based on the 'Min. CSI' setting).
2. Any additional specific 'Context Genes' you add below.
The final network is a combined view. Choose an Interaction Source (pathways or protein interactions) and optionally compare CSI scores with a Baseline Cell Type.

Maximum number of selected genes.
Select a context for the baseline cell.
Select a context for the target cell.
Target Cell for CSI:  plasmacytoid dendritic cell, human (CL0001058)

 Legend
Nodes (Genes):
 Query Gene
Node size also reflects Target Cell CSI magnitude.
Node Color (Target Cell CSI in specific network):
 Very High
 High
 Medium
 Low
 Very Low
 N/A or Not Sig.
Edges (Interactions):
 STRING (Protein-Protein)
 ONTOLOGY (Shared Pathway)
 Colors vary by pathway category; default arrow applies.

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## Summary The [plasmacytoid dendritic cell, human](/details-cell/CL0001058) is a specialized immune cell type known for its potent ability to produce Type I interferons in response to viral infections. The provided gene significance data, which emphasizes expression specificity, reveals that beyond their canonical immune functions, these cells are uniquely defined by a highly specific and active core cellular machinery. The top markers are dominated by genes involved in fundamental processes such as iron metabolism ([FTH1](/details-gene/2495), [FTL](/details-gene/2512)), endoplasmic reticulum stress response ([HERPUD1](/details-gene/9709)), and high-level protein synthesis and processing ([SRP14](/details-gene/6727), [PABPC1](/details-gene/26986)). This suggests that the identity of a [plasmacytoid dendritic cell, human](/details-cell/CL0001058) is not only defined by its specialized immune receptors and signaling pathways but also by a distinct metabolic and protein-handling infrastructure likely poised to support its massive secretory function upon activation. ## Key Characteristics and Function **Overall**, the gene expression profile of [plasmacytoid dendritic cells, human](/details-cell/CL0001058) highlights a cell state optimized for high metabolic activity and robust protein production. The top-ranking genes can be grouped into several key functional clusters: * **Protein Synthesis, Processing, and Translation:** A large number of the most specific markers are core components of the translational and RNA processing machinery. This includes genes like [SRP14](/details-gene/6727) (involved in targeting proteins for secretion), [PABPC1](/details-gene/26986) (poly(A)-binding protein), RNA helicase [DDX5](/details-gene/1655), and several eukaryotic translation elongation factors ([EEF1B2](/details-gene/1933), [EEF1D](/details-gene/1936)). The high specificity scores (`csi_z`) for these genes indicate that the expression level of this machinery is a uniquely defining feature of pDCs, consistent with their role as professional secretory cells. * **Metabolism and Bioenergetics:** The data reveal a strong and specific signature of mitochondrial and metabolic activity. Multiple subunits of the cytochrome c oxidase complex ([COX4I1](/details-gene/1327), [COX2](/details-gene/4513), [COX1](/details-gene/4512), [COX7C](/details-gene/1350)) and ATP synthase ([ATP5F1E](/details-gene/514), [ATP5MG](/details-gene/10632)) are among the top markers. This points to a distinct reliance on oxidative phosphorylation to meet the high energetic demands of their immune functions. Critically, the top marker [FTH1](/details-gene/2495) and the related [FTL](/details-gene/2512) gene, which encode ferritin heavy and light chains, underscore a specialized role for iron metabolism and sequestration, a process essential for mitochondrial function and redox balance. * **Cellular Stress and Cytoskeletal Organization:** The second most specific marker, [HERPUD1](/details-gene/9709), is an ER-stress-induced protein. Its high specificity suggests that pDCs are constitutively adapted to manage a high level of protein folding stress, which would be essential for their capacity to rapidly synthesize and secrete vast quantities of interferons. Additionally, the specific expression of cytoskeletal components like [MYL12A](/details-gene/10627), [CFL1](/details-gene/1072), and [MYL6](/details-gene/4637) may indicate unique requirements for cell motility, morphology, and immunological synapse formation. * **Core Immune Identity:** The presence of [B2M](/details-gene/567) (Beta-2-microglobulin), a component of MHC class I molecules, as a highly specific marker confirms their role in antigen presentation, a hallmark of dendritic cells. * **Defining by Absence (Anti-Markers):** The lack of significance for genes like [SERPINF2](/details-gene/5345) (alpha-2-plasmin inhibitor) and [PADI4](/details-gene/23569) (implicated in neutrophil extracellular trap formation) helps to distinguish pDCs from other hematopoietic lineages involved in coagulation or distinct innate immune effector functions. ## Clinical Significance and Contextual Roles While the analysis is based on an **Overall** context, the unique genetic signature of [plasmacytoid dendritic cells, human](/details-cell/CL0001058) carries significant clinical implications. pDCs are central players in the pathogenesis of autoimmune diseases like systemic lupus erythematosus (SLE), where their chronic production of Type I interferons drives inflammation. The remarkable specificity of iron-handling genes ([FTH1](/details-gene/2495), [FTL](/details-gene/2512)) is particularly noteworthy. Iron dysregulation is a known feature of chronic inflammation and autoimmunity, and this data suggests pDCs may have a unique role in this process. Manipulating iron availability could potentially modulate pDC function and their pathogenic activity in disease. Furthermore, the high ranking of the ER stress gene [HERPUD1](/details-gene/9709) points to the unfolded protein response (UPR) as a critical pathway in pDCs. The UPR is essential for managing the protein-folding load during interferon production. This pathway could represent a vulnerability; targeting the UPR might be a therapeutic strategy to selectively dampen the excessive interferon production by pDCs in autoimmune settings. ## Potential Mechanisms and Research Directions 1. **Hypothesis:** The highly specific expression of ferritin subunits ([FTH1](/details-gene/2495), [FTL](/details-gene/2512)) suggests that a specialized iron sequestration mechanism is fundamental to the metabolic priming of pDCs. This iron-handling capacity may be essential not only for fueling the high energetic cost of interferon synthesis via mitochondrial respiration but also for protecting the cell from iron-induced oxidative stress during intense activation. * **Surprising Findings:** The most defining gene marker for this key interferon-producing cell is not a component of the interferon pathway itself, but rather a protein involved in iron storage. This implies that the metabolic state, particularly iron homeostasis, is a more unique identifier for this cell type than its canonical functional modules in this dataset. * **Testable Questions:** Does pharmacological iron chelation or genetic knockdown of [FTH1](/details-gene/2495) in human pDCs alter their metabolic profile (e.g., oxidative phosphorylation rates) and subsequently impair their ability to produce IFN-alpha in response to TLR9 agonists like CpG-A? 2. **Hypothesis:** The high specificity score of the ER stress-responsive gene [HERPUD1](/details-gene/9709) indicates that pDCs maintain a constitutively active or 'poised' unfolded protein response (UPR) pathway. This state of readiness may be a key adaptation that allows for the exceptionally rapid and massive production of secreted interferons upon viral sensing, bypassing the need for de novo induction of the entire stress-response machinery. * **Surprising Findings:** An ER stress-associated gene shows greater expression specificity than many classical immune signaling molecules. This suggests that managing the consequences of protein synthesis is a more unique biological challenge for pDCs than the initial sensing of pathogens, which utilizes pathways shared by other immune cells. * **Testable Questions:** Using single-cell proteomics or targeted transcriptomics, do resting [plasmacytoid dendritic cells, human](/details-cell/CL0001058) exhibit higher basal levels of [HERPUD1](/details-gene/9709) and other key UPR proteins (e.g., XBP1s, BiP) compared to conventional dendritic cells or B cells? Does inhibition of the UPR pathway prior to stimulation disproportionately affect interferon production in pDCs?