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
4 steps involved in therapeutic research involving pathogens
- Identify and label molecules in complex mixtures
- Serotype pathogens
- Identifying cell types
- Humanised antibodies used in therapy
What product found in the body can indicate transplant rejection
OKT3 which binds to CD3
What do B cells recognise
Soluble native antigens
What do T cells recognised
Cell-associated processed antigens
What chromosome encodes Major Histocompatibility proteins
Chromosome 6
What are MHPs important in
Graft rejection
What are Major Histocompatibility proteins also known as
HLA molecules
What property do all MHPs have
Very polymorphic
What is the role of MHP
Initiate T cell responses
Role of MHC I
Display antigen to CD8 (cytotoxic T cells)
Role of MHC II
Display antigen to CD4 (helper cells)
What three cells express MHC II
- Macrophages
- Dendritic Cells
- B cells
What happens to a viral-infected cells so that the CD8 recognises peptide bound to MHC I
Viral proteins broken down in cytosol
Peptides transported to ER and bind to MHC I
What happens to T helper cells physiologically when they interact with MHC II
- Macrophage/Dendritic cell/B cell internalises and breaks down foreign material
- Peptides bind to MHC II in endosome which are displayed on cell surface
- Antibody production
How do cytokines act
Locally
Role of IL-1
Induces Inflammation, fever and activates leukocytes
Role OF IL-2
Stimulates T, B and NK cell growth
Role of IL-4
Induces IgE production and TH2 differentiation
Role of IL-8
Induces neutrophil chemotaxis
Role of IL-10
Down-regulates TH1 cytokines and MHCII expression
Where are IL-1 made
Macrophages, endothelial and epithelial cells
Where are IL2 made
T cells
Where are IL-4 made
Mast cells and TH2 cells
Where are IL-8 made
Macrophages, endothelium, fibroblasts, keratinocytes
Where are IL-10 made
Monocytes and TH2 cells
Role of INF gamma
Activates macrophages and NK cells
Increases MHC II expression
Where are INF made
TH1 and NK cells
Where are TNF alpha made
T, macrophages and NK cells
Role of TNF alpha
Activates neutrophils and endothelial cells
Wasting
What do TH1 cells produce (cytokines)
IL2, INF-gamma, TNF-beta
What do TH2 produce (cytokines)
IL4,5,6,10,13
What do TREG cells produce and why
IL-10 and TGF-beta - to down-regulate or act against the other cytokines
How does infection protect against allergy
Promotes IL-10 and TGF-beta production to reduce number of TH1 and TH2 (increase in TREG)
