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T-cell Activation by Dendritic Cells
Dendritic cells (DCs) are crucial antigen-presenting cells that initiate adaptive immune responses by activating T-cells. They capture pathogens, process antigens, and present them via MHC molecules to specific T-cells in lymph nodes. This activation leads to the differentiation of T-cells into effector cells, orchestrating targeted immune responses against diverse threats like bacteria and viruses.
Key Takeaways
Dendritic cells are central to initiating adaptive immunity.
MHC Class II presents extracellular antigens to CD4+ T cells.
MHC Class I presents intracellular antigens to CD8+ T cells.
Cross-presentation allows DCs to activate CD8+ T cells from exogenous antigens.
T-cell cross-priming enables simultaneous CD4+ and CD8+ activation.
How do Dendritic Cells activate T-cells during a bacterial infection?
When a bacterial infection occurs, specialized dendritic cells (DCs), such as Langerhans cells, play a critical role by actively phagocytosing extracellular bacteria. This process involves engulfing the pathogens and processing their antigens into peptides. These peptides are then loaded onto Major Histocompatibility Complex Class II (MHC Class II) molecules. The DC subsequently migrates to regional lymph nodes, where it presents these MHC Class II-peptide complexes to naïve CD4+ Helper T cells. This interaction, combined with co-stimulatory signals, leads to the robust activation and differentiation of CD4+ T cells into effector subsets like Th1 or Th17. These effector cells secrete vital cytokines, including IL-2, which are essential for helping macrophages and B cells mount an effective immune response against the bacterial threat.
- Pathogen source: The primary source of antigens is extracellular bacteria, which are found outside host cells.
- DC action: Dendritic cells perform phagocytosis, engulfing bacteria, followed by maturation to become effective antigen presenters.
- Presentation pathway: Antigens are processed and presented via the MHC Class II pathway, designed for exogenous antigens.
- T Cell interaction: Naïve CD4+ Helper T cells recognize these MHC Class II-peptide complexes.
- Outcome: Activation leads to effector CD4+ T cells (Th1/Th17), cytokine release (e.g., IL-2), and crucial help for macrophages and B cells.
When do Dendritic Cells use classical MHC Class I activation for intracellular threats?
Dendritic cells employ classical MHC Class I activation when they are directly infected by an intracellular pathogen, such as a virus or specific bacteria. In this scenario, the pathogen replicates within the DC's cytosol, generating foreign proteins. These endogenous antigens are then processed through the proteasome and loaded onto MHC Class I molecules within the endoplasmic reticulum. The DC presents these MHC Class I-peptide complexes on its surface to naïve CD8+ Cytotoxic T cells in the lymph nodes. This crucial interaction triggers the activation and differentiation of CD8+ T cells into effector cytotoxic T lymphocytes (CTLs). These potent CTLs then specifically target and kill infected cells, including the original infected dendritic cell, to eliminate the intracellular threat.
- Pathogen source: The antigens originate from an intracellular virus or bacteria that directly infects the dendritic cell.
- DC action: The virus infects the DC, leading to the production of foreign proteins within the cell's cytosol.
- Presentation pathway: Antigens are presented through the MHC Class I pathway, which handles endogenous proteins.
- T Cell interaction: Naïve CD8+ Cytotoxic T cells specifically recognize and bind to these MHC Class I complexes.
- Outcome: Activation results in effector CD8+ CTLs, which then kill infected cells, including the original dendritic cell.
What is cross-presentation and how does it activate CD8+ T cells during viral infections?
Cross-presentation is a unique mechanism enabling dendritic cells to activate CD8+ Cytotoxic T cells using exogenous antigens, typically derived from viral debris or dying infected cells. Instead of direct infection, the DC phagocytoses these external sources of viral proteins. These exogenous antigens are then remarkably diverted into the MHC Class I pathway, a process termed cross-presentation. This allows the DC to present viral peptides on MHC Class I molecules to naïve CD8+ T cells in the lymph nodes. The activated effector CD8+ CTLs subsequently exit the lymph node, migrating to infected tissues to locate and efficiently kill other virally infected cells throughout the body, thereby controlling viral spread.
- Pathogen source: Antigens are derived from viral debris or dying infected cells, which are external to the DC.
- DC action: The dendritic cell phagocytoses the infected cell material, acquiring exogenous viral proteins.
- Presentation pathway: These exogenous antigens are uniquely processed and presented via the MHC Class I pathway through cross-presentation.
- T Cell interaction: Naïve CD8+ Cytotoxic T cells are activated upon recognizing these cross-presented MHC Class I complexes.
- Outcome: Effector CD8+ CTLs are generated, which then exit the lymph node to kill other virally infected cells.
How does T-cell cross-priming lead to coordinated adaptive immune responses?
T-cell cross-priming describes a sophisticated scenario where a single dendritic cell simultaneously activates both CD4+ and CD8+ T cells, even when encountering an extracellular pathogen without direct infection. The DC efficiently captures antigens through phagocytosis or pinocytosis. It then processes and loads microbial peptides onto both MHC Class II (via the exogenous pathway) and MHC Class I (via the cross-presentation pathway) molecules. This coordinated presentation, alongside essential co-stimulatory molecules, ensures a robust and comprehensive T-cell activation. The outcome is a powerful adaptive response where activated CD4+ T cells provide crucial help, and activated CD8+ T cells become potent killers, working together to effectively clear the infection.
- Context: A single dendritic cell encounters an extracellular pathogen without being directly infected.
- Step 1: Antigen Capture: The DC efficiently captures microbial antigens through phagocytosis or pinocytosis.
- Step 2: MHC Class II Loading: Processed antigens are loaded onto MHC Class II molecules via the exogenous pathway.
- Step 3: MHC Class I Loading: Simultaneously, some exogenous antigens are diverted for MHC Class I loading through cross-presentation.
- Result: This leads to coordinated adaptive priming of both T-cell subsets.
- MHC II + Microbial Peptide -> Activates Naïve CD4+ T cells, initiating helper functions.
- MHC I + Microbial Peptide -> Activates Naïve CD8+ T cells, preparing for cytotoxic action.
- Co-stimulatory Molecules (B7/CD80/CD86): Essential for full activation of both CD4+ and CD8+ T cells.
- CD4+ Activation: Differentiates into Effector TH cells, which secrete crucial Cytokines like IL-2.
- CD8+ Activation: Differentiates into Effector CTLs, which actively seek and kill infected cells.
- Cooperation: CD4+ T cells provide vital "help" signals, enhancing the potency and longevity of CD8+ killer cells.
Frequently Asked Questions
What is the primary role of dendritic cells in immunity?
Dendritic cells are professional antigen-presenting cells, acting as sentinels of the immune system. They efficiently capture, process, and present diverse antigens to T-cells in lymph nodes, thereby initiating robust adaptive immune responses and developing specific immunity against various pathogens.
What is the difference between MHC Class I and MHC Class II presentation?
MHC Class I molecules present endogenous antigens, derived from proteins synthesized inside the cell, primarily to CD8+ T cells, crucial for viral infections. Conversely, MHC Class II molecules present exogenous antigens, acquired from outside the cell, to CD4+ T cells, typically for bacterial threats.
Why is cross-presentation important for viral immunity?
Cross-presentation is vital because it allows dendritic cells to activate CD8+ T cells against viruses even when the DC itself is not directly infected. This mechanism is essential for initiating a potent cytotoxic T-lymphocyte response to effectively clear virally infected cells and control disease spread.
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