Podcast
Questions and Answers
Which of the following scenarios would MOST effectively induce T cell-independent B cell activation?
Which of the following scenarios would MOST effectively induce T cell-independent B cell activation?
- Interaction with a T helper cell that has been pre-activated by an antigen presented on an MHC class I molecule.
- Exposure to a protein antigen presented by MHC class II molecules on dendritic cells.
- Crosslinking of multiple BCRs by a large, repeating antigen, such as a polysaccharide. (correct)
- Direct engagement of the B cell receptor (BCR) by a soluble protein antigen that is subsequently internalized and presented to T cells.
An experiment introduces a modified antigen that binds to the T cell receptor (TCR) but is unable to trigger the downstream signaling cascade normally associated with T cell activation. What is the MOST likely outcome?
An experiment introduces a modified antigen that binds to the T cell receptor (TCR) but is unable to trigger the downstream signaling cascade normally associated with T cell activation. What is the MOST likely outcome?
- Enhanced T cell activation due to increased TCR occupancy.
- T cell anergy or tolerance due to incomplete activation signals. (correct)
- T cell activation will proceed, but the response will be delayed due to the modified antigen.
- Normal T cell activation and subsequent cytokine production.
A researcher is investigating potential therapeutic targets to enhance the immune response in cancer. Which of the following strategies would MOST directly amplify T cell activation through co-stimulation?
A researcher is investigating potential therapeutic targets to enhance the immune response in cancer. Which of the following strategies would MOST directly amplify T cell activation through co-stimulation?
- Blocking the interaction between the TCR and the peptide-MHC complex.
- Administering a drug that inhibits MHC class I expression on tumor cells.
- Introducing a soluble form of CTLA-4 to outcompete CD28 binding.
- Using an antibody that blocks the interaction between PD-1 on T cells and PD-L1 on tumor cells. (correct)
A patient with a genetic defect lacks the ability to produce CD80 and CD86 proteins on their antigen-presenting cells (APCs). Which of the following immune responses would be MOST significantly impaired?
A patient with a genetic defect lacks the ability to produce CD80 and CD86 proteins on their antigen-presenting cells (APCs). Which of the following immune responses would be MOST significantly impaired?
A novel immunosuppressant drug selectively inhibits the production of IL-2 by T cells. Which of the following consequences is MOST likely to occur in a patient treated with this drug?
A novel immunosuppressant drug selectively inhibits the production of IL-2 by T cells. Which of the following consequences is MOST likely to occur in a patient treated with this drug?
A researcher is studying the interaction between a T helper cell and a B cell during a T cell-dependent B cell activation. If the MHC class II molecule on the B cell is mutated such that it cannot bind to the T cell receptor, what is the MOST likely outcome?
A researcher is studying the interaction between a T helper cell and a B cell during a T cell-dependent B cell activation. If the MHC class II molecule on the B cell is mutated such that it cannot bind to the T cell receptor, what is the MOST likely outcome?
Which of the following BEST describes how dendritic cells bridge innate and adaptive immunity during an initial immune response to a novel pathogen?
Which of the following BEST describes how dendritic cells bridge innate and adaptive immunity during an initial immune response to a novel pathogen?
A patient has a mutation that impairs the function of their pathogen recognition receptors (PRRs) on macrophages. How would this MOST likely affect T cell activation?
A patient has a mutation that impairs the function of their pathogen recognition receptors (PRRs) on macrophages. How would this MOST likely affect T cell activation?
In the context of T cell activation, what is the PRIMARY role of adhesion molecules such as LFA-1 and ICAM-1?
In the context of T cell activation, what is the PRIMARY role of adhesion molecules such as LFA-1 and ICAM-1?
If a researcher wants to investigate the signaling pathways activated downstream of the T cell receptor (TCR), which of the following experimental approaches would provide the MOST direct insights?
If a researcher wants to investigate the signaling pathways activated downstream of the T cell receptor (TCR), which of the following experimental approaches would provide the MOST direct insights?
Flashcards
Lymphocyte Activation
Lymphocyte Activation
T and B cell activation requires intracellular signaling cascades that activate transcription factors, leading to gene transcription, cytokine production, maturation and proliferation.
T Cell Activation Signals
T Cell Activation Signals
APCs present extracellular antigens via MHC class II molecules. Signal one involves TCR recognition, while signal two involves CD28 and CD80/86 interaction.
B Cell Activation Pathways
B Cell Activation Pathways
B cells activate either by direct interaction with TI antigens (T cell-independent) or through MHC class II-TCR interaction (T cell-dependent).
T Cell Activation Signals (Detailed)
T Cell Activation Signals (Detailed)
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CD4+ T Cell Activation
CD4+ T Cell Activation
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Professional APCs
Professional APCs
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Antigen Recognition (T vs. B cells)
Antigen Recognition (T vs. B cells)
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Antigen Presentation
Antigen Presentation
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Co-stimulation in T cell Activation
Co-stimulation in T cell Activation
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IL-2 Role in T Cell Activation
IL-2 Role in T Cell Activation
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Study Notes
- Activation of T and B cells, both lymphocytes, is central to humoral and cell-mediated immune responses.
- Activation requires signal initiation, leading to intracellular signaling cascades.
- These cascades activate transcription factors, enabling gene transcription, cytokine production, maturation, and proliferation.
- B cell receptors (BCRs) bind antigens on cell-bound or soluble molecules, unlike T cell receptors (TCRs) which recognize antigen-MHC complexes.
- Detection and interpretation of environmental signals are crucial for both lymphocytes in directing immunological responses.
T Cell Activation
- Extracellular antigens are presented by MHC class II molecules on antigen-presenting cells (APCs).
- TCRs recognize the antigen-MHC class II complex, forming a weak bond.
- Adhesion molecules stabilize cell interactions.
- CD28 on T cells interacts with CD80/86 on APCs, providing a second signal.
- Two signals are required to activate T cells.
- Cytokines released by APCs support the differentiation and proliferation of effector T cells.
B Cell Activation
- B cells can be activated by T cell-independent or T cell-dependent interactions
- Independent activation involves direct interaction with TI-1 and TI-2 antigens (lipopolysaccharides and repetitive epitopes, respectively)
- Dependent activation requires BCR recognition of the antigen and MHC class II binding to the TCR.
- In T cell-dependent activation, T cells present antigens to B cells originally presented by an APC.
Similarities between B and T cell activation
- Compartmentalization of function within receptor subunits
- Activation by membrane-associated protein tyrosine kinases
- Assembly of large signaling complexes with protein–tyrosine-kinase activity
- Recruitment of several signal-transduction pathways
Antigen Presentation
- Early studies showed cell-mediated responses could be induced by native, denatured organisms, or parts of microbes
- Certain cells can bridge the activation of innate and adaptive immune responses.
- APCs express class II MHC and deliver a co-stimulatory signal.
- Cells displaying peptides with class I MHC molecules to CD8+ T cells are target cells.
- Dendritic cells, macrophages, and B cells are classified as professional APCs.
- APCs bridge innate immunity in humoral (antibody production) and cell-mediated (cell lysis) responses
Professional APCs
- Dendritic cells, macrophages, and B cells are the three professional APCs.
- APCs activate T cells and indirectly or directly activate B cells.
- B cells are also APCs, capable of processing and presenting antigens to T cells.
- All display antigens on class II MHC molecules.
- APCs originate in the bone marrow.
- B cells develop from lymphoid progenitor cells in the bone marrow.
- Immature B cells leave the bone marrow, mature in peripheral lymph nodes, and start displaying antigens on MHC molecules.
- Dendritic cells may derive from myeloid progenitors too.
- Macrophages differentiate from monocytes that originate from myeloid progenitors in the bone marrow.
Process of pathogen detection by APCs
- Macrophages patrol physical barriers.
- They recognize pathogens through pathogen recognition receptors (PRRs) like toll-like receptors.
- Dendritic cells also have PRRs and can detect foreign substances.
- Upon detecting a pathogen invasion, APCs secrete cytokines, which act as alarm signals.
- Cytokines recruit more macrophages and dendritic cells to the injury site.
- Dendritic cells engulf pathogens using dendrite-like processes.
- Pathogens are degraded inside the cell, and fragments are displayed on class II MHC molecules.
- Displaying pathogen-derived antigens signals a hostile environment to T and B cells.
CD4+ T Cell Activation
- Antigen Presentation: APCs (dendritic cells, macrophages, B cells) capture and process antigens. Antigens are presented on MHC class II molecules.
- TCR Interaction: CD4+ T cells use TCRs to recognize peptide-MHC class II complexes.
- Co-stimulation: CD80/86 on APCs interact with CD28 on T cells for additional signals.
- Signal 1 (TCR Engagement): Initiates signaling cascades in the CD4+ T cell.
- Signal 2 (Co-stimulation): CD28 on the CD4+ T cell engages with CD80/86 on the APC to enhance T cell activation.
- Signal 3 (Cytokine Signaling): APCs release cytokines like IL-12 to further stimulate the CD4+ T cell.
- Cytokines influence CD4+ T cell differentiation into Th1, Th2, Th17, or Treg cells.
- Clonal Expansion: Activated CD4+ T cells produce IL-2, promoting clonal expansion and differentiation into effector and memory cells.
TH1 cells
- CD4+ T cells respond to intracellular pathogens by recruiting and activating phagocytic cells.
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