Immune System 4 Flashcards
Describe the activation process of Cytotoxic T cells:
Cytotoxic T cell activation involves:
- Binding to antigen presentation (clonal selection).
- Potential involvement of costimulation and cytokine secretion.
How can we maximally activate the Cytotoxic T Cells?
Maximal activation requires contributions from Helper T cells, specifically IL-2 and other cytokines, stimulating full clonal expansion resulting in effector and memory cells.
What will Cytotoxic T Cells do once activated?
Activated effector cytotoxic T cells circulate and will recognize virus infected cells.
After Recognition, what do Cytotoxic T Cells Release? (2)
With recognition effector cells:
Release perforin
- Similar to MAC; creates a channel for intracellular entry.
Release granzymes.
- Digestive enzymes enter via perforin-created channel.
What is the Final Step after Cytotoxic T Cells complete the Recognition stage and release their contents?
- Virus infected cells self destruct (can lose a lot of cells depending on how many are infected).
- Virus released into extracellular where other defenses can more easily attack
What is the Role of Regulatory T Cells?
Used to be called suppressor T cells.
Suppress immune responses to keep from over-reacting (provides some balance).
- If immune system reacts excessively could cause attack on own cells and lead to autoimmune disease.
- Helps provide self-tolerance.
- Help control inflammation by acting as negative regulators.
- Help with accepting organ transplantation.
What is the exact mechanism used by Regulatory T Cells to Suppress immune responses to keep from over-reacting?
four
- They Inhibit T Cell Proliferation and some Cytokine
Production - Produce Inhibitory Cytokines
- React to IL-2 in a Negative Feedback
- Prevent some Costimulation.
Describe the activation process of B cells:
B cell activation involves:
- Direct binding to pathogen antigens (clonal selection).
- Initiation of clonal expansion.
How are B Cells Maximally Activated?
Maximal activation requires the helper T cells contributions (IL-2 and other cytokines) to stimulate full B cell clonal expansion; some effector and some memory cells.
What are the 2 pathways Effector B Cells can take?
- Proliferation: B cells make more B cells
- Differentiation: B cells differentiate into plasma cells that secrete antibodies for specific antigen
What are Examples of Direct attacks that result “directly” from pathogen antigen-antibody binding?
3
Neutralization
Agglutination
Precipitation
Direct Antibody Attack:
What is Neutralization?
Neutralization:
Blocks pathogen attachment to healthy cells or interferes with pathogen chemical reactions
Direct Antibody Attack:
What is Agglutination?
Agglutination:
clumping when pathogen antigen and antibody bind (results in easier phagocytosis by large complex size being easier to recognize)
Direct Antibody Attack:
What is Precipitation?
Precipitation:
Comes out of solution when pathogen antigen and antibody bind (easier phagocytosis by visibility).
What is an Indirect Antibody Attack?
Indirect attacks by antibodies result from more than just pathogen antigen-antibody binding
2 cases below start with antibody binding to pathogen
antigen and acting like opsonization (“marker” on pathogen).
Indirect Attack
What is Enhanced Phagocytosis?
Enhanced phagocytosis occurs when a phagocyte, possessing the correct receptor, attaches to the stem end of an antibody. This attachment forms a bridge between the pathogen and phagocyte, making phagocytosis easier due to the physical binding
Indirect Attack
What is Antibody-Dependent Cellular Cytotoxicity (ADCC)?
In Antibody-dependent cellular cytotoxicity (ADCC), an NK cell with the correct receptor attaches to the stem end of an antibody. This attachment forms a bridge between the pathogen and the NK cell. The NK cell then releases cytotoxic chemicals to destroy the pathogen.
What characterizes indirect attacks by antibodies, and how does the “Classic” complement pathway contribute to this process?
Indirect attacks involve more than just pathogen antigen-antibody binding. The “Classic” complement pathway starts with antibody binding to a pathogen antigen, acting as opsonization. C1 complement protein, initially circulating inactive, activates by binding to the antibody binding site on the side of the stem end of the antibody.
How does the “Classic” complement pathway initiate, and what is the role of C1 complement protein in this process?
The “Classic” complement pathway initiates with antibody binding to a pathogen antigen, acting like opsonization. C1 complement protein, initially circulating in an inactive state, activates by binding to the antibody binding site on the side of the stem end of the antibody.
What is the cascade of events triggered by the activation of C1 in the “Classic” complement pathway?
Activation of C1 in the “Classic” complement pathway initiates a cascade of complement protein activations. Once this cascade activates C3, the pathway follows the same steps as the “alternative” complement pathway, including the insertion of C3b to enhance phagocytosis and the formation of the Membrane Attack Complex (MAC).
