Innate, Adaptive, Humoral and Cell-mediated Immunity Flashcards
Describe how humoral immunity works
- Antigen binds to antibody on B lymphocyte
- Plasma cells
- Antibodies produced
Define Humeral Immunity
Defence against extracellular bacteria and secondary viral infections
What are the ‘fab’ regions of the antibody
The variable region that bind to antigen on pathogen
What are the ‘fc’ regions of the antigen
The ‘constant’ regions which bind to receptors of phagocytes and NK cells - eliminate antigen)
Why are the chains in an antibody called heavy and light
Light - 25kD
Heavy - 50kD
Are the variable and constant regions encoded by the same exon
Nope
How does the genome give rise to specific antibody shapes
Multiple V regions in the genome can recombine and mutate during B cell differentiation
What antibody is IgG similar to
IgD
What antibody has a similar shape to IgG and IgD but can be found as a dimer instead
IgA
Structure of IgD
The two polypeptide chains that make the constant (Fc) region have three amino acids each
The two polypeptide chains that make the fab region have two amino acids each
Structure of IgG, IgA and IgD
The two polypeptide chains that make the constant (Fc) region have two amino acids each
The two polypeptide chains that make the fab region have two amino acids each
Structure of IgM
Pentamer of ‘Y-shaped’ antibodies joined together by J chain in the centre
Role of IgG
Secondary and Memory responses
How is IgG inherited
Cross the placenta
Role of IgM
Primary responses
Role of IgA
Protects mucosal surfaces
Role of IgE
Allergy and response to parasitic infections
How does the level of IgM and IgG vary from primary to secondary response
- IgM increases rapidly during primary and there’s a delayed increase of IgG as specific antibodies are made. Both reach the same conc peak before declining
- Upon secondary infection, IgG levels increase earlier and more rapidly than IgM and reach almost triple the conc. IgM reaches the same peak as the primary infection conc. wise.
How do antibodies protect against infections
- Neutralise toxins (IgG and IgA)
- Immobilise microbes (IgM)
- Prevents binding to host cells
- Form complexes
- Enhance innate mechanisms (complement system activation)
- Bind Fc receptors
Result of binding to phagocytic Fc receptors (IgG and IgA)
Enhances phagocytosis
Result of binding to Mast Cell Fc receptors (IgE)
Release of inflammatory mediators
Result of binding to NK cells (IgG) Fc receptors
Enhanced killing