4. Immunology (2) Flashcards
Adaptive immunity cells need _____ presented to them.
antigens
What are MHC Class 1 molecules? (2)
- MHC I are present on all NUCLEATED cells in our body.
- Typically, white blood cells have lots of MHC I, hepatocytes less, and red blood cells almost none (probably why malaria finds refuge in them).
What are MHC Class 2 molecules?
MHC II are found ONLY on specialized antigen presenting cells = B lymphocytes, dendritic cells, macrophages.
What is extracellular bacteria?
What is the process of exocytosis?
What is the function of MHC Class 1 molecules? (4)
What is the function of MHC Class 2 molecules? (3)
How do MHC II molecules and B cells assist Helper T cells to produce cytokines? (3)
Antibodies have TWO functions done by 2 separate parts of the antibody molecule:
- Recognition of antigen (antigen binding site) by the variable region
- Effector function is done by the constant region
B-cell receptor does not have these effector functions because the C region is buried in the membrane —>
its role is to activate B cells.
The different suffixes of the antibody isotypes denote the different types of heavy
chains the antibody contains, with each heavy chain class named alphabetically: α
(alpha), γ (gamma), δ (delta), ε (epsilon), and μ (mu). This gives rise to : (5)
IgA, IgG, IgD, IgE, and IgM.
Mature Naïve B-cells (those that have not encountered their antigen) express ____ and ____ on their surface.
IgM
IgD
When they encounter their antigen and are activated class switching occurs. Class switching is the process whereby an activated B cell changes its antibody production from IgM to either___,____, or _____ depending on the functional requirements.
IgA, IgG, or IgE
In the end, most of our Ig are represented by ____.
IgGs
Activation of B cell results in: (3)
- Clonal proliferation
- Secretion of IgMs
- Ig Class switching from IgM to IgG or IgE or IgA
Fill in the arrows.
C1
IgG and IgM
What is the classical complement pathway?
What is the C1- inhibitor? (4)
- C1-inhibitor is an acute-phase protein that circulates in blood.
- The levels rise ~2-fold during inflammation.
- It stops the classical pathway.
- It also limits spontaneous activation of C1 in the plasma.
What is the result of the deficiency of the C1-inhibitor? (2)
- Deficiency of this protein is associated with hereditary angioedema (“hereditary angioneurotic oedema”), or swelling due to leakage of fluid from blood vessels into connective tissue.
- Deficiency of C1-inhibitor permits localised vasodilation and increased vascular permeability. In its most common form, it presents as marked swelling of the face, mouth and/or airway that occurs spontaneously or to minimal triggers (such as mild trauma), but such swelling can occur in any part of the body. In 85% of the cases, the levels of C1-inhibitor are low, while in 15% the protein circulates in normal amounts but it is dysfunctional.
What is the result of the deficiency of the C1-inhibitor? (2)
- Deficiency of this protein is associated with hereditary angioedema (“hereditary angioneurotic oedema”), or swelling due to leakage of fluid from blood vessels into connective tissue.
- Deficiency of C1-inhibitor permits localised vasodilation and increased vascular permeability. In its most common form, it presents as marked swelling of the face, mouth and/or airway that occurs spontaneously or to minimal triggers (such as mild trauma), but such swelling can occur in any part of the body. In 85% of the cases, the levels of C1-inhibitor are low, while in 15% the protein circulates in normal amounts but it is dysfunctional.
Primary immune response vs Secondary immune response
Occurrence:
Primary immune response vs Secondary immune response
Response:
Primary immune response vs Secondary immune response
Response:
Primary immune response vs Secondary immune response
Lag phase: