Immune System 4

Question 1

Why do Th cells have coreception

Answer 1

To prevent accidental activation, making sure its for a good cause

Question 2

Antibody methods (names only), there are 6

Answer 2

Neutralizing antigen
Agglutinating antigen
Precipitating antigen
Opsonization
Activating the complement
Antibody-dependent cellular cytotoxicity

Question 3

Neutralizing antigen

Answer 3

One of the ways antibodies look out
Messing or physically blocking or finding a way to prevent the antigen from binding to cells, like if you block teh receptor it can never bind to the cell to infect/infiltrate it
Not destroy, just neutralized the function and harmful aspect

Question 4

Agglutinating antigen

Answer 4

Another way antibodies look out
Basically antibodies can bind to two antigens, not chemically linking them together but anchoring them to each other
“Glues” them together such that they cant easily infiltrate the blood stream and have to stay put for phagocytosis
Not killing, just preventing them from going to harm

Question 5

Precipitating antigen

Answer 5

Another way antigens look out
If you have a small and soluble antigen, you can make the antibodies bind to it, making it heavy and bulky and less soluble so it cant move as effectively through blood stream, slowing it down enough to eventually be destroyed
Very similar to agglutination

Question 6

Opsonization (antibody)

Answer 6

Another way for antibodies to look out
Antibodies bind to the specific epitope of the bacteria and it serves as a marker to any passing phagocytes that this is a cell we want destroyed
Specific to microbe

Question 7

How do phagocytes recognize opsonization (by an antibody not a complement) as an indicator that that cell must go

Answer 7

The recognize the general part of the antibody, the Fc region (crystallizable fragment region), the heavy chains
Is therefore non specific since it recognized the general part

Question 8

Complements in the specific vs non specific branches of immunity

Answer 8

Non-specific: Alternate pathway: the pathogen surfaces, the complement is activated, it opsonizes the pathogens (marks it), pathogen is more visible to phagocytes for consumption
Specific: Classical pathway: requires an antibody-antigen complex, the complement is activated, leads to killing of pathogen

Question 9

Classical pathway for complement, the details

Answer 9

Antibody-antigen complex
Complement proteins (just found circulating in fluid), first C1, is going to be activated due to presence of complex
Seeing an activated complement will inspire others to activate, causing a cascade of activations
Result: some of these complement proteins will form a pore in the antigen, the MAC, content of cell will flow out and bacterial cell will die

Question 10

MAC

Answer 10

Membrane attack complex, opens pore in antigen to let its guts leak out

Question 11

Antibody-dependent cellular cytotoxicity

Answer 11

Another way antibodies look out
Done by NK cells, but in a specific way, not non-specific like in other immune category
Recognizes the FC region of the antibody, has receptors for it, can bind to it and that will trigger its destructive tendency
Releases granzyme and perforin, perforin will make small pores and granzymes will go in a kill

Question 12

NK cells in adaptive vs non-specific

Answer 12

Non-specific: chose to kill based on MHC1 receptor, if it was downregulated or modified smtg was wrong and it would destroy the cell, can hit cancer too
Specific: NK cells also have Fc binding site, for antibodies (the general part), so if it sees an antibody in a cell, basically as an opsonin, it can recognize and destroy
Different recognitions

Question 13

Antibody dependent cellular cytotoxicity applications in cancer

Answer 13

If an antobody can be produced for a cancer cell, be purified and then reinserted into the body, the antibody can bind to the cancer cells so that the NK cells can destroy them

Question 14

How can we acquire antibody-mediated immunity (brief)

Answer 14

Actively or passively, and from there naturally or artificially

Question 15

Acquiring antibody-mediated immunity actively

Answer 15

Active implying that you own personal immune system went through the process of creating the antibodies and the memory cells and the whole process, provides long term immunity
Can be done naturally: someone sneezes on you, you get infected and you fight it off
Artificially: you’re purposefully exposed to antigen, like in a vaccine

Question 16

Acquiring antibody-mediated immunity passively

Answer 16

Passively meaning you did not go through the process of making your own antibodies and memory cells, so you will only be protected short term
Can be done:
Naturally: when a mother passes down her IgG antibodies through placenta for example, baby didn’t synthesize but they still protect it
Artificially: you recieve a serum containing antibodies, like how they would treat Ebola

Question 17

Vaccine

Answer 17

Small quantities of living of dead antigen (older way of doing it), maybe small antigenic molecules derived from pathogen, just enough so that your body can produce memory cells for it to help for future exposure

Question 18

Antibodies passed on from mom to baby

Answer 18

In utero (fetus): IgG, passes through placenta
Post-birth: IgA, in the mothers milk

Question 19

Convalescent serum

Answer 19

Serum of someone who has already developed antibodies is purified to being almost just antibodies, injected to give you a head start and a fighting chance
Hopefully without antigen

Question 20

Gaining immunocompetence

Answer 20

When a lymphocyte (B or T cell) has to develop its specific antigen receptor (not open to recognizing all antigens and cells)

Question 21

What does the antigen receptor on a B cell look like

Answer 21

Like an antibody, 2 heavy and 2 light chains
Sam region will bind to antigen (light chain tip)

Question 22

What lymphocytes have to gain immunocompetence

Answer 22

All
B cells, cytotoxic T cells and helper T cells

Question 23

Process of B cells gaining immunocompetence (starting in bone marrow)

Answer 23

B cells are born an raised in the bone marrow
As the B cell is maturing, its developing its B cell receptor on its surface, can then go to secondary lymph organ (once receptor is developed and mature
At this point, they all have the same generic DNA (in example its heavy chain) coding for the B cells receptor, with the VDJ sections (potential specific region) and the constant region
Undergoes VDJ recombination where RAGs (recombination activating genes) will splice out different regions of the VDJ to narrow down its specificity to one
This occurs for the heavy and light chain DNAs, then tdT s can add more diversity too
Once specific like this, theres no going back since these changes are made at the DNA level

Question 24

VDJ recombination

Answer 24

V, D and J are each sections in the variable region of the DNA in B cells (or any of the lymphocytes) and they each have a bunch of different options, all present in the initial mature B cell (capable of recognizing anything)
VDJ recombinations goal is to narrow it down to have a combination that only creates receptors for 1 antigen

Question 25

RAGs

Answer 25

Recombination activating genes Will basically splice out most of the VDJ DNA to narrow it down

Question 26

How many combinations exist in the process of gaining immunocompetence

Answer 26

10000 combinations can arise from the heavy chain DNA 200 from the light chain DNA

Question 27

Role of TdTs

Answer 27

TdTs, terminal deoxynucleotidyl transferase Adds single nucleotides to ends of VDJ section Since codons work in groups of 3, adding one or two will completely shift the reading frame, adding even more diversity

Question 28

Considering the concept of gaining immunocompetence, how can B cells produce different types of antibodies

Answer 28

All antibodies produced by a given cell will have the same variable region, its the constant region that changes between class of antibody So the constant region can change for IgMs compared to IgGs, but the variable wont

Question 29

What will the first and second exposures to a new antigen be like in terms of what class of antibody is being produced?

Answer 29

First: once B cells are activated and start producing antibodies, they will produce IgMs (say 5) and then production will shift to IgGs (will also peak at 5) Second: Memory cells have been made, there has been prior exposure, IgMs will still be produces first (peaking at 5) but once the memory cells get kickstarted and shift to IgGs, they’ll fly and peak at like 20, making the second exposure easier

Question 30

Can lymphocytes create receptors to self-antigens if they can make any combination?

Answer 30

No, they will not create antibodies to self antigens like MHC1 and 2

Question 31

Immune tolerance

Answer 31

Idea that any lymphocytes made to recognize self antigens during fetal and post natal life will be destroyed, cuz that could really be an issue. Done in 2 ways Clonal deletion: killing the self reactive cell Clonal anergy: permanently deactivating the cell, will find some sort of way to block this lymphocyte from getting the second signal or cytokines it needs to be fully activated Without full activation its useless This prevents autoimmune responses

Question 32

T cell tolérance in utero (sélective process)

Answer 32

Example: helper T cells If it cannot recognize MHC2, it dies (necessary during APC presentation of antigen) If it recognizes MHC1, it dies (cuz it would want to kill self cells) 95% of T cells are destroyed, but most effective way considering we can recognize basically anything