Immune System, Lecture 4 Flashcards
B Cell - activation
- B cell activation with direct binding pathogen antigen (clonal selection) starting clonal expansion
- maximal activation requires the helper T cell contributions (IL-2 and other cytokines) to stimulate full B cell clonal expansion; some effector and some memory cells
- some effector B cells differentiate into plasma cells that secrete antibodies for specific antigen
- remember: proliferation is B cells making more B cells differentiation is B cells making plasma cells (and then antibodies)
my notes:
- clonal selection is pathogen binding to the variable end of the B cell (the one that has the right variable end “lock and key”)
- some become memory cells for storage and also to plasma cells which then becomes differentiation (antibodies will get released into circulation and go looking for pathogens to bind to)
Antibody - attacks (direct)
direct attacks - result “directly” from pathogen antigen-antibody binding
- neutralizations: blocks pathogen attachment to healthy cells or interferes with pathogen chemical reactions
- agglutination: clumping when pathogen antigen and antibody bind (easier phagocytosis by complex size)
- precipitation: comes out of solution when when pathogen antigen and antibody bind (easier phagocytosis by visibility)
my notes:
- clumping (two things bind together / antigen and antibody) just means larger structure which makes it easier to recognize which enhances phagocytosis
- taken small pathogen that was hiding and make it larger when it binds to antibody so it is more visible
- precipitation makes it more visible - when the antibody and antigen bind together you make them more visible which enhances phagocytosis (antigen is invisible until bound with antibody)
Antibody - attacks (indirect)
indirect attacks - results from more than just pathogen antigen-antibody binding
- 2 cases below start with antibody binding to pathogen antigen and acting like opsonization (“marker” on pathogen)
enhance phagocytosis
- phagocyte with correct receptor attached to stem end of antibody
- forms bridge between pathogen and phagocyte to make phagocytosis easier as physically bound
antibody-dependent cellular cytotoxicity (ADCC)
- NK cell with correct receptor attaches to stem end of antibody
- forms bridge between pathogen and NK cell
- NK cells releases cytotoxic chemicals to destroy pathogen (once it binds)
- not much of a specific recognition anymore cause of all of the stem ends are the same in each category (with 5 categories only have to recognize between 5 stems ends)
- variable end is attached to pathogen and stem end is attached to either phagocyte or NK cells depending on what you are looking at
Antibody - attacks (“classic” complement pathway - indirect)
indirect attacks - results from more than just pathogen antigen-antibody binding
“classic” complement pathway
- starts with antibody binding to pathogen antigen and acting like opsonization (“marker” on pathogen)
- C1 complement protein circulating inactive; activates by binding antibody binding site for C1 on side of stem end of antibody
- triggers a cascade of complement protein activations starting from C1
- once cascade activates C3 “classic” complement pathway is same as “alternative” complement pathway (insertion of C3b to enhance phagocytosis / formation of MAC)
- difference from “alternative” complement pathway is starting steps
my notes:
- classic starts with activation of C1 and alternative begins with activation of C3
- antibody need to be attached to pathogen to make C1 binding site available (C1 cannot bind if antibody is floating free on its own)
- complement proteins are just plasma proteins that float inactive
Immunity - previous exposure to antigen?
antibody production
- following first contact (primary response)
◦ slow (several weeks) response
◦ smaller numbers specific antibodies
◦ limited time in blood
- subsequent encounter (secondary response) by same antigen:
◦ quicker response (almost instantly as seen on
graph)
◦ larger numbers specific antibodies
◦ lasts longer in blood
- secondary response, mediated by memory cells, is one of the key features distinguishing innate and adaptive immunity
- confers greatly enhanced immunity toward subsequent infection
my notes:
- first time we see a pathogen and encounter a antigen on that pathogen we take a bit more time to give an immune response (adaptive system is slower system / loses its effectiveness after a month), however it produced memory cells that will be stored in spleen or lymph nodes for example that will be there for subsequent encounter
- even though secondary drops within a few months the number of antibodies are still pretty elevated (memory cells have a hand in this)
- sometimes memory may only last a few weeks depending on pathogen (the amount of time they stay variable - weeks, months, decade, lifetime)
Immunity - active
active - 2 forms - exposure to antigen
- active natural: exposure to antigen by chance (ex. touch a doorknob ~ some surface has a pathogen on it)
- active artificial: deliberate exposure to antigen (vacine)
◦ vaccine: small quantities living or dead pathogens,
toxins, or harmless antigenic molecules derived
from microorganism or its toxic
my notes:
- active natural is by chance so someone coughs in your face, the antigen goes past your defense
- vaccine are all based on little chunk of material that codes for that spike protein and once formed it blocks the ability for that protein to get in potentially (active artificial)
- active you are exposed to antigen and then antigen would have to be used to develop antibodies whereas passive you just directly give antibody
Immunity - passive
passive - 2 forms - directly transfer or already formed antibodies
- passive natural - antibody transfer mother to infant
◦ mother and fetus: IgG can move across placenta
◦ breast-fed child: IgA in breast milk can move
across intestinal lining
‣ important early protections as antibody
synthesizing relatively poor
- passive artificial - antibody transfer person to person (injection)
◦ rapidly dangerous or fatal conditions where no
time to wait for active immunity to be developed
(used with hepatitis A, snake bites, rabies)
- preformed antibodies offer immediate protection but limited lifespans (weeks or months)
◦ they do not produce memory cells because we
are passed that step to form them (works more
for someone with immediate risk and needs
antibodies quickly ~ not good for longterm use)
my notes:
- immune system is relatively slow to develop so that is why the transfers from mother to infant is important (IgG / IgA)
- with active artificial you are injecting antigen / with passive artificial you are injecting antibody directly (take them from someone who already had antibodies and transfer them to someone else)
Immunity, Exercise and Stress
strong ties - immunity, exercise and stress
stress
- depressed immune responses - visits to student health over term a good indicator
- under stress, less likely to eat well or exercise regularly - 2 enhancers of immunity
- also critical to immunity: adequate sleep and relaxation / optimistic outlook / good relationships with people
exercise
- inverted “J” shape curve of immune function and relation to disease susceptibility
◦ moderate - enhanced immune responses -
reduced susceptibility
◦ exhaustive - depressed immune responses -
increased susceptibility with potential for
immunosuppression that may be prolonged
‣ with proper training (sufficient rest and
recovery) can be avoided
→ it is not saying do not do exhaustive training, just do it at an appropriate number and get adequate rest in between, so you are not overtraining (a good balance between easy and hard workouts)
