The Immune Response Flashcards
Latent Phase (aka: lag or inductive)
After initial exposure to an immunogen it is the period of time before Ab can be detected
Exponential Phase (aka: logarithmic)
Ab begins and rate of production increases resulting in exponential increase in Ab concentration
Steady State
Peak Ab concentration
Decay (aka: decline)
Decline in Abs followed by a time when a small amount of Ab can be detected
Secondary Response (aka: memory)
After initial exposure to Ag
How does 2ndary response compare to primary?
Faster - Shorter lag time Higher rates of Ab synthesis Higher peak of Ab Longer persistent response Predominance of IgG Higher affinity to Ab Requires less Ag
B-cells
Express surface Ig
Each only allowed to express a SINGLE variable region
What is repertoire?
The total population of B-cells make up the repertoire of Ab specificities
How are Ags seen
Seen by B-cells–> and those cells with COMPLEMENTARY Ig sequence will respond
How are T-cells involved in this process?
They aid in BC proliferation
Clonal Expansion
A single BC can produce up to 1000 daughter cells in 10 days
- As immune response continues there is an increase in affinity of Ab produced
- Class switching occurs (IgM–>IgG)
How can increase affinity be explained?
As a selective expansion of those clones w/ the highest affinity to Ag
-As [Ag] drops only those clones w/ the highest affinity will be stimulated
Helper T-cells - CD4+
Recognize diff set of Ags than BCs
Most Ags it reacts to are proteins or peptides
How do TCs react with Ag
React with Ag on the surface of the APC and in response to Ag (with MHC) and co-stimulatory molecules
-TCs proliferate and produce factors that stimulate BCs
How do BCs respond to TCs
- Many daughter BCs will react to TC derived factors and differentiate into plasma cells
- Other TC factors involved in switching IgM production to IgG
- Some of the daughter cells wont differentiate and will become memory cells
T-independent Ags
- Not all immunogens require TC help to produce an immune response
- Generally polymorphic molecules having a large # of repeating subunits that can cross link to Ig on BC
- Others are polyclonal activators of BCs (usually provided by TCs) through TLR
APCs
Initiate interaction w/ Ag by endocytosis or phagocytosis
How can this be enhanced?
Interaction w/ complement
Pre-existing Ab
With specific receptors that recognize pathogens
APC after uptake of Ag
Is followed by Ag-processing - where Ag is digested
and
Ag presentation - Ag is deposited on the surface of the presenting cell
This is a HIGHLY immunogenic form of Ag
How is Ag presented
As MHC/Ag complex
What do lymphocytes respond to?
To Ag that is presented w/ self MHC
Apart from Ag processing, what must APCs provide?
Co-stimulatory signal
- cell surface Ags are considered CRITICAL for an immune response
- ->most imp CD28 (on TC)-B7(on APC)
Does presentation of Ag w/o co-stimulation produce immune response?
NO
A APC must …
1- take up and process Ag
2- have MHC C2 Ag on its surface
3- present Ag w/ MHC C2 Ag
4- provide co-stimulatory signal (B7)
B-cells are capable of …
1- processing Ag
2- expressing MHC C2 Ag
3- expressing co-stimulators
What is a toxin?
Proteins that will kill you
-no amount that wont
-will not induce immune response
If you somehow survive - you are NOT immune and STILL need vaccine
What is a toxoid?
Chemically modified protein that will induce immune response
-antigenitically same as toxin, but wont kill you
Hepten Carrier
Hepten seen by BC
Carrier seen by TC
