Dendritic Cell Infection
Dendritic Cell Infection - Related Videos
11:39
T Cells Capture Bacteria by Transinfection from Dendritic Cells
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Cited by 2 •
2016
Here a protocol is presented to measure bacterial capture by CD4+ T cells which occurs during antigen presentation via transinfection from pre-infected dendritic cells (DC). We show how to perform the necessary steps: isolation of primary cells, infection of DC, DC/T cell conjugate formation, and measurement of bacterial T cell transfection.
08:11
Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
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Cited by 1 •
2015
Unlike cell-free HIV-1 particles, infected CD4+ T cells are effectively sensed by plasmacytoid dendritic cells (pDCs). This manuscript describes a method where peripheral blood mononuclear cells (PBMCs) or isolated pDCs are co-cultured with HIV-1 infected T cells to evaluate innate sensing by pDCs as assessed by release of type-I IFN.
07:14
A CFSE-based Assay to Study the Migration of Murine Skin Dendritic Cells into Draining Lymph Nodes During Infection with Mycobacterium bovis Bacille Calmette-Guérin
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Cited by 10 •
2016
An assay in mice to track cell migration from skin to draining lymph node is described which enables the characterization of skin Dendritic cells mobilized to the lymph node after footpad infection with Bacille Calmette-Guérin.
03:44
siRNA-Based Inhibition of Autophagy in Herpes Simplex Virus-Infected Immature Dendritic Cells
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2025
This video demonstrates a small interfering RNA (siRNA)-based technique to interfere with autophagic flux. A siRNA targeting FIP200 mRNA is introduced into monocyte-derived immature dendritic cells (iDCs) using electroporation, causing the knockdown of FIP200 expression and leading to the inhibition of nuclear lamin disruption via autophagy. Upon adding herpes simplex virus (HSV), the nuclear egress of viral progeny is inhibited due to the absence of lamin disruption via autophagic flux.
09:04
Isolation of Mouse Lung Dendritic Cells
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Cited by 17 •
2011
A highly purified preparation of mouse lung dendritic cells is described. Specific emphasis is given to the isolation of conventional dendritic cell subset.
FAQs
Receptor engagement determines how a pathogen is internalized and which intracellular compartment it reaches. Interactions with pathogen-associated molecules can trigger uptake into endosomes or entry into the cytoplasm, initiating innate signaling while also placing microbial material in locations where antigen processing may occur. These early routing decisions therefore influence both cellular defense and the information later presented to lymphocytes.
Endosomal and cytoplasmic uptake routes provide different settings for innate signaling and antigen processing. Examining which compartment contains pathogen-derived material helps researchers relate intracellular location to the cell’s subsequent immune behavior. This distinction matters because a pathogen’s route may affect whether dendritic cells process microbial components effectively and continue toward productive antigen presentation.
Some pathogens interfere with dendritic-cell maturation, antigen presentation, or antiviral defenses after entering the cell. Such disruption can change how efficiently pathogen-derived peptides reach major histocompatibility complex molecules and may influence the cell’s ability to coordinate adaptive immunity. Studying these effects helps explain how infection can weaken or redirect immune responses rather than simply trigger them.
A study can follow the sequence from pathogen recognition and cellular entry through intracellular localization, innate signaling, antigen processing, and later immune-cell behavior. Investigators can then examine whether infected dendritic cells mature, display pathogen-derived peptides, and migrate toward lymphoid tissues. Organizing observations along this sequence connects early host-pathogen interactions with downstream adaptive immune consequences.
Researchers investigate dendritic cell infection to clarify host-pathogen biology and to understand how microorganisms influence antigen presentation and adaptive immune responses. The findings can support vaccine development, infectious disease research, and efforts to improve immune-based therapies. This topic is especially relevant when infection changes dendritic-cell maturation, migration, or antiviral defenses.
The process links events inside an infected dendritic cell to immune coordination beyond that cell. After pathogen-derived peptides are processed and displayed on major histocompatibility complex molecules, dendritic-cell migration to lymphoid tissues can help connect microbial recognition with adaptive immune activation. If a pathogen disrupts these steps, the resulting immune response may be altered.