Flashcards in Things To Know Deck (106)
Do CD4+ Th cells bind to extracellular or intracellular?
They bind to Extracellular pathogen-specific peptide epitopes via TCR
Does CD8+ T cells bind to extracellular or intracellular
They bind to intracellular pathogen-specific peptide epitopes via TCR
What kind of structure does a TCR bind to?
It binds to a peptide antigen which will require processing from an APC in order to bind
What does a BCR bind to in terms of structure?
It will bind to a tertiary structure of a protein, carb, lipopolysach, polysaccharide
It does not require processing in order to bind
What is the point of the prevnar vaccine in terms of what it activates?
It is a polysaccharide Ag which is conjugated to a protein reactive material (CRM 197) this is important because it allows for Bcell and Tcell cooperation because the Bcell will process the protein and act as an APC to recruit Tcells and cause a larger immune response leading to increased efficacy of the shot.
What does INF-gamma cause for isotype switching?
IgM to IgG
What does IL-4 cause in terms of isotype switching
IgM to IgE
What does IL-5 cause in terms of isotype switching?
IgM to IgA
What is affinity maturation?
It’s when you have isotype switching which leads to production of specific antibodies that are able to bind to the pathogen with higher affinity compared to the ones that were originally created
What is CAR t-cell treatment
It’s when you pull a patients T-cells out of their peripheral blood and you engineer the T-cell or CAR t-cell to recognize the surface tumor antigens so it can kill them
They CAR T cell has increased signaled so it causes a higher response to the cancer
What is the role of IL-2 in activation of T-cells?
It will drive the proliferation and differentiation of activated T-cells
What do Th1 cells secrete?
Which stimulates phagocytosis and killing of microbes by macrophages, inflammation
IgM to IgG
What do Th2 cells secrete ?
IL-4 causes IgM to IgE, big in allergic rxn and eosinophil killing of helminth
IL-5 which changes IgM to IgA
What do Th17 cells produce?
Involved in inflammation and autoimmune diseases MS, IBD
What does the complement system consists of?
Serum proteins and cell surface proteins that interact to generate products for elimination of microbes
What part of immunity is our complement system apart of
Innate and humoral immunity
People who lack C3 will have a high chance of getting a ton of infections
Which two pathways of the complement system are innate immunity and why?
It’s the Alternative pathway and the lectin pathway
the reason is because it does not require and antibody in order to be started
Alternative = activated by the microbe
Lectin = activate by presence of Mannose
The classical is humoral because you need to have an IgG or IgM bound to the microbe in order to start
What are the steps of T-cell activation?
Step 1: binding of peptide Ag with MHC to a TCR
Step 2: Binding of costimulitory factors to increase T-cell proliferation and differentiation
CD28 binds to B7 (CD80/CD86)
CD40L bind to CD40
Also CD3 which is part of TCR which increase stimulating effects
This all increase the amount of NFAT, NFkb and AP1 which are transcription factors to make more and different types of T-cells
What are the central tolerance types of immune tolerance
Happens in the bone marrow for Bcells and happens in the thymus for Tcells
Deletion = apoptosis and just kill the cell
Receptor editing = in bcells to change what it does
Development of Tregs = release inhibitory cytokines IL-10 and TGF-Beta to stop the function of Tcells
THESE WORK ON IMMATURE LYMPHOCYTES
What are the types of Peripheral tolerance in immological tolerance?
Clinal anergy = do not have function responses (would be like not activating CD28 to bind with B7 so it results in a lower response of Tcell)
Deletion = apoptosis
Suppression - using Tregs to release inhibitory cytokines (IL-10, TGF-Beta) to suppress the action of the lymphocytes
THESE WORK ON MATURE LYMPHOCYTES
What type of lymphocytes is most susceptible to tolerance
What is negative selection when it comes to immune tolerance?
When a lymphocytes has a high affinity for self antigen is will be negatively selected and killed off
They may also become Tregs (CD4+,CD25+), which will release suppressive cytokines (IL-10, TGF-beta) in the peripheral
What is me ant by positive selection of lymphocytes
It means it has a low affinity for self Ag meaning it will be saved by TCR receptor and allowed to mature and enter the peripheral system
What is the role of Orencia (abatacept)?
it mimics CTLA-4 which is going to cause the blocking of B7 (CD80/86) from binding to CD28 which means there will not be a reaction of the Tcell
It’s an immunosuppressive drug in the use for RA
Where are Tregs created
Primarily in the thymus
The IL-10 and TGF-B suppresses activation and effector functions of sel-reactive and pathogenic lymphocytes in periphery
ALSO BLOCKS ACTIVATION OF MACROPHAGES
***if we didn’t have these we would have a lot of autoimmune diseases
What happens to B lymphocytes when it comes to peripheral tolerance
When a B-cell reacts to a self antigen it doesn’t cause the activation of Th cells (because it cant package the self antigen into a MCH) this leads to the Bcell to be very ineffective and unresponsive (anergic) and will die by apoptosis
What are the main ways we have central tolerance in Bcells?
B cells that target Self antigen in the bone marrow have to fates
1: receptor editing where we change the antigen receptor so that it is no longer self reactive
2: dies by apoptosis with negative selection (deletion)
How can we use immune tolerance to help with allergies?
We inject the pt with the allergies or have them eat them (peanuts) this will cause the antigen to seem more like a self antigen and will cause our T and B cells to become desensitized to them and no longer react
We have to start with low amounts and slowly increase the amount we give them
How does autoimmune diseases happen?
The self-Ag is not expressed in the thymus or the concentration is way to low. This will allow Tcells that are auto reactive to escape the thymus where they will then start to react with our bodies Self-Ag and cause autoimmune diseases
Type 1 diabetes, SLE (systemic lupus, Type III hypersensitive rxn)