Flashcards in B Cells & Antibodies Deck (54):
Which chromosome has the gene for the heavy chain of B cell receptors?
What happens if both genes (on respective Chromosome 14s) fail to produce full-length Heavy Chain proteins for the BCR?
-the cell undergoes apoptosis
What happens if the B cell produces light chains that don't match the heavy chain on its BCR's?
the cell undergoes apoptosis
Which portion of the B cell receptor signals thenucleus when the receptor recognizes an antigen?
What must happen to B cell receptors before they can signal B cell activation?
-clustering of BCR's
-Crosslinking of B cell receptors**
-a signal from a helper T cell if necessary **
When does a naive/virgin B cell become experienced?
-when it is activated after they meet their respective cognate antigens
How are B cells activated independent of helper T cells?
-only needs 1 signal
-in response to certain antigens, enough BCR's will cross-link to activate the cell
***T cells only recognize protein antigens, so this system allows us to respond to carbs and fats
What is the "unnatural" way in which B-cells can be activated?
-a mitogen binds to molecules on the B cell's surface, which are not BCR's
-molecules cluster together
-this allows clustering of BCR's
**does not depend on cognate antigen. parasites use mitogens to distract the immune system (irrelevant antibodies are produced) e.x. Shistoooooo
What are the three steps of B cell maturation?
**order of the steps can vary and be skipped
What is the class switching maturation step in B cells?
-switching of class of antibody produced
What is the result of class switching?
-part of the antibody that binds to antigen (Fab) remains the same
-Fc region is changed
Which class of antibodies are first produced by naive B cells?
-also IgD, but we don't know what it does
What do IgM antibodies do to complement?
-activates complement cascade
-brings together C1 complexes, which then act as a C3 convertase (much C3b, wow)
**C1 has inhibitor attached, bring 2 together and inhibitors fall off
What is the significance of IgM binding to foreign antigens before activating complement?
-some bacteria have walls that are resistant to complement binding
-IgM allows for complement activation in these cases
Where does C1 bind to IgM?
the Fc region
Can IgG activate complement?
Yes, but it can only bind one copy of C1 a piece
-two IgG molecules must bind an invader close together to activate complement
Which IgG class is best at activating complement and serves as a bridge for Natural Killer cells?
Which IgG class is good at opsonizing invaders for macrophage ingestion?
Which antibody can cross the placental barrier, and provides the fetus protection until production of its own antibodies?
**IgG is very good at fighting viruses
What is the most abundant antibody class in the human body?
***IgG is most abundant in blood
What do IgA antibodies do?
-guard the mucosal surfaces of the body
-can coat pathogens in the intestine
-has 4 Fab regions, so good at collecting pathogens into clumps large enough to be cleared with feces
Can IgA antibodies fix complement?
**this is good, elsewise our mucosal surfaces would be in a state of constant inflammation, which is not fun
What causes anaphylactic shock?
-mast cell degranulation
-when people are exposed to allergens they make lots of IgE to that allergen, and mast cells have IgE receptors
-triggers mast cell degranulation
-on second exposure to allergen, IgE abs already bound to mast cells bind to the allergen, clustering receptors, triggering degranulation
Why do B cells switch classes?
-with a common cold we don't want to depend on IgM, but need IgA
-with a parasitic infection we want IgE
What class of antibody do B cells switch to in an area rich in IL-4 & 5? What kind of invader are they fighting?
Good for parasites
What class of antibody do B cells switch to in an area rich in IFN-alpha? What kind of invader are they fighting?
Bacteria and viruses
What class of antibody do B cells switch to in an area rich in TGF-beta? What kind of invader are they fighting?
What is somatic hypermutation?
-Genese for Fab region have a high mutation rate
-When B cell switches from making IgM antibodies, mutation rate drastically increases
-mutates the antigen binding region of Fab
What are the three possible outcomes of somatic hypermutation?
-affinity of Fab to cognate antigen is unchanged
-affinity is increased
-affinity is decreased
Do B cells activated independent of T cells undergo class switching and somatic hypermutation?
Through what surface receptor do Helper T cells interact with B cells to activate them?
What happens to old and damaged proteins in a cell?
-they are cut by proteasomes then displayed by the cell's class I MHC molecules
What are the three main steps in class I MHC display?
1. Generation of the peptide by the proteasome
2. Transport of peptide to ER
3. Binding of peptide to groove in MHC I molecule
Where are class II MHC's loaded with peptides?
What does the invariant chain do?
-Fills the MHC II molecule to prevent it from picking up other peptides
**important b/c ER is full of endogenous proteins, which if loaded into MHC II they would display same kinds of peptides as class I MHC
What Does HLA-DM do to the MHC II molecule?
-removes the invariant chain once the MHC II reaches the endosome
What cells read Class I and II MHC's respectively?
Class I = Killer T cells
Class II = Helper T cells
Which class of MHC is found on antigen presenting cells?
both class I and II
What two things must happen for a T cell to become activated?
-T cell must recognize its cognate presented by an MHC molecule
-Must also receive a co-stimulatory signal (provided by APC's)
What are the three types of antigen presenting cells?
-Activated Dendritic cells
-Activated B cells
What signals activate dendritic cells?
-cytokines from neutrophils and macrophages
-Cellular receptors (ex: TLR) which recognize molecular patterns of invaders
What do dendritic cells use TLR4 to sense?
=a component of (gram negative?) bacterial cell walls
What happens to dendritic cells when they're activated?
-no longer spit fluid back into environment
-Leave home tissue and travel via lymphatics to nearby lymph nodes
Produces B7, which along with MHC I & II, it uses to activate virgin T cells
How do dendritic cells recruit their own replacements?
-once activated, they produce chemokines to cause monocytes to leave the blood and differentiate into dendritic cells
What is the difference between dendritic cells and macrophages?
-Dendritic cells don't kill
-Macrophages don't travel
-macrophages not as good at antigen presenting
If the macrophage doesn't travel to the lymph node, what is its role in antigen presentation?
-Dendritic cells activate virgin T cells, Macrophages present antigens to keep the activated T cells going
What is the advantage of B cells over other APCs?
-They can concentrate antigens for presentation
Why would it be dangerous for Cytotoxic T cells to recognize antigens that aren't presented on an MHC?
-if uninfected cells have some debris from a dead virus stuck on their surface, then the T cell would kill the healthy cells
How does complement activated B cells?
-C3b opsonizes enemy
-B cell has complement receptors
-bound complement receptors will bring BCR's together and activate the B cell
***helps innate immune system determine if invader is dangerous
What do IgM antibodies look like?
like 5 IgG antibodies stuck together by their Fc regions
What do IgA antibodies look like?
Like 2 IgG antibodies held together at Fc region with a clip
What is the utility of the structure of IgA?
-allows for transport across the intestinal wall into the intestine
-also keeps antibody safe from digestive enzymes
What does B7 produced by dendritic cells do?
-serves as second signal to activate virgin T cells, along with MHC I & II