adaptive immunity 1 Flashcards
How is an immunity developed?
what happens first? what does it stimulate? how do you recover? aftermath?
Most previously unseen infections progress through – Initial infection stimulating an immune response Innate & Adaptive (Acquired) – Recovery due to immune activity – Lasting acquired immunity Specific Often for life
Innate response
spped?
acts on?
The Innate Response to new infections is
FAST
acts on PRE DETERMINED NON SELF SIGNALS
SOMETIMES can be primed for intense re activation ( INNATE MEMORY
Adaptive response
speed?
key feature? (2)
The Adaptive Response to new infections is
SLOW
and SELECTS for SPECIFIC SIGNALS
and generates MEMORY
T and B cells
made where?
key feature?
Each T or B cell is made in the bone marrow with
a randomly assigned antigen binding specificity.
An individual has at any one time > 100,000,000
individual cells each with a different specificity
T and B cells can have the same specificity
T cell development
what migrates where?
what happens here?
Naïve (Double negative) T lymphocyte will migrate to thymus gland for processing where it will either become
CD8+ Cytotoxic T lymphocyte (CTL)
CD4+ Helper T lymphocyte (Th)
Destroyed if strongly recognise self antigens (Central tolerance)
B cell development
where? what does it express?
Naive B lymphocyte will develop and mature in Bone Marrow To express a single epitope antibody used as a receptor
ENDOGENOUS PATHWAY of T cell priming
what is infected? what happens to this cell? what is presented?
what recognises this? what happens and what is produced?
what happens to the infected cell? what happens to the activated cell? (2)
Antigen from virus will infect an antigen presenting cell. The viral proteins in the cytoplasm will be detected and processed. Viral antigens are presented with MHC Class I molecule on cell surface
ONLY CD8+ T cell recognises antigen, becomes cytoxic and begins to make cytokines (recognise MHC Class I)
THe infected cell is destroyed by the cytotoxic cell via chemicals. Also, CTL (same as CD8+) will proliferate making memory cells and CTL cells looking for cells with presented antigen hence specifity (and memory)
EXOGENOUS PATHWAY of T cell priming
what happens to antigen?c by what? what happens to the anitgen? presented with?
what recognises this and what does it release?
Antigen of a pathogen will be engulfed by a dendrtic cell or macrophage into a vesicle. The antigen will be processed into small peptides. Antigen is presented with MHC Class II molecule on cell surface and T - Helper cells (TH) recognises the presented antigen. TH (CD4+) cell becomes primed and release cytokines looking for a B cell
EXOGENOUS PATHWAY of B cell priming
B cell activation (T cell independent)
what kind of pathogen must it be?
what does activation lead to?
what is this pathway restircted to and what can it lead to?
Pathogen containing multiple identical antigen
epitopes eg. Lipopolysaccharide (LPS) able to strongly activate B cell (rare)
Activation initiates proliferation with some cells being
memory cells
Activated B cells convert to Plasma cells and begin making antibody
This pathway is restricted to specific antigens and is
not checked for tolerance CAN lead to problems
such as Toxic Shock Syndrome
EXOGENOUS PATHWAY of B cell priming
B cell activation (T cell dependent)
how does this avoid auto immunity?
what activates B cell? effect of this?
Antibody production required co stimulation with a Th cell that was already screened against self thus auto immunity is avoided
B & Th cell interaction activates B cell
Activation initiates B cell proliferation with some cells
being memory cells and some Committed to antibody production
Basic antibody structure
what kind of protein is it?
anitgen binding sites?
what is between the binding sites?
what kind of shape is made?
what holds the chains together?
specific bond between with amino acids? type of bond?
what is key about the light and heavy chains?
describe the light chains ( 2 types)
describe the heavy chains - what determined Ig classes?
Antibody = Immunoglobulin = Glycoprotein
2 identical antigen binding sites
A Hinge ’H’ region flexible spacer between binding
sites
4 polypeptide chains held together by non covalent interactions and by disulphide crosslinks between cysteine a.a residues into a Y shaped molecule
2 identical Light ‘L’
Either kappa ( κ ) or lambda λ
Never both
2 identical Heavy ‘H’ ( Red Blue )
Have carbohydrates attached in Golgi body during assembly
Sequence of Fc section determines 5 Ig classes (isotypes)
Antibody fragments
what is FaB?
what is Fc?
Protease cleavage generates large fragments called
Fab (antigen binding)
Fc (crystallisable)
Fab - variable region binds antigen
Fc - constant region binds to receptors on phagocytes,
activates complement
2 structure of IgM
what is the difference between the 2?
- Monomer of basic sub unit
B cell receptor
Extra Heavy Chain domain that is membrane bound in the B cell
2.Pentamer of basic sub unit in plasma ( secreted Ig)
Contains a J chain a polypeptide involved in pentamer polymerisation
Benefits of pentamer IgM
larger hence can bind to more antigens, can complement in different ways
mops up things + works better
Function of antibody classes: IgG
what is this made by?
special about this and baby?
what is it very good at?
what does it act as? what do these cells recognise?
how long can it be present in body? what may this indicate?
the major class overall (75% of all Ig) the major class made by secondary responses only class able to cross the placenta and protect developing fetus (small enough to pass and as foetus doesnt make own antibodies and needs protection)
very good at activating complement via classical
pathway (removing the
acts as an “ opsonin ” inducing phagocytosis
– Fc region recognised by “Fc receptors” on surface of
immune cells. eg , neutrophils and macrophages
It can be present for long periods in the serum thus IgG antibodies may indicate past exposure and not current infection !!!
