Ch 18: Adaptive Specific Host Defenses Flashcards
Adaptive immunity displays specificity and memory
Specificity:
=> means the adaptive immune system can recognize slight differences between pathogens (more accurately between antigens)
Memory:
=> menas that the adaptive immune system changes over time, responds to the second challenge by the same pathogen more quickly but in different, better ways
Primary response
the response which follows the first exposure to a pathogen of antigen
secondary response
the response whihc follows further exposures to the same (specific) pathogen or antigen
adaptive immunity depends on lymphocytes
B and T cells
lyphocytes can rearrange their DNA after exposure
B lymphocytes
mature in the bone marrow (the bursa in birds) and secrete antibodies (Ab)
most antibodies circulate in the blood, B cells and Ab are called humoral defence
T lymphocytes
mature in thymus
secrete cytokines and interleukines (Th cells) or kill virus infected cells (CTLs)
cellular defence or immunity
Antigens (Ag)
An Ag is a unique biological structure found only on one type of pathogen
Viral Ag
all viruses have capsids, only influenza viruses have haemagglutinin proteins in the capsid, only influenze strain A H3N3 has the type H3 haemagglutinin
Protein Ag
proteins are the best Ag followed by carbs, nucleic acids, and lipids (most immunogenic)
protein Ag stimulate both humoral and cellular function
Carbohydrate Ag
stimulate only humoral immunity
Lipid and Nucleic acid Ag
are only antigenic if attacherd to a protein or other moleucle called a hapten
epitope
the smallest part of an antigen recognized by an AB or a T cell receptor
large Ag have many epitopes
Antibodies
glycoproteins produced and secreated by B cells
all antibodies are at least bivalent
5 classes// isotypes
IgM
the first Ab produced
is a pentamer of IgG like structyures so has 10 heavy and 10 light chains
is the Ab of teh primary respose
food at afflutination but does not bind Ag very strongly
activates complement
some B cells become memory cells
IgG
cirvulatory Ab, second type produced
bivalent, can bind two identical antigens
consistant domains interact with receptors on macrophage and neutrophils to cause opsinization and complement activation
oGG is the Ab of the secondary response
higher affinity than IgM
opsinizes, activates complement, agglutinates
IgA
Ab agaisnt multicellular pathogens, also involved with allergies
secreted onto mucosal surfaces and binds pathogens there
dimer of bivalent Ab, so it has 4 heavy and 4 light chains
IgD
B cell surface Ab, B cell receptor
Antibody strucutre IgG
4 polypeptides, 2 heavy and 2 light chains
each chain is made up of variable and consistant domains
the variable domain from one light chain and a variable domain from one heavy chain combine to form the antigen binding site
constant domains interact with receptors on macrophage and neutrophils to cause opsinization and complement activaiton
light chains have 1 variable domain and 1 constant domain
Heavy chains have 1 variable and 3 constant domains
B cells and antibodies
Ab are only produced by B cells
As B cells amture, they undergorandom genetic rearrangement in the genes for Ab
=> in the varaiable region, generates a unique specificity for each Ab
each B cell produces a unique Ab
B cell activation
IgD as the B cell receptor
when the B cell is activated by binding Ag to the IgD then IgM Ab are produced and secreted
B cells require T cells to activate
Neutralization
Binding of antibodies to toxins// viruses to prevent them from attaching to receptors
IgG and IgM
binding of antibodies to bacterial cells to prevent them from attaching to epithelial and other cells
binding of antibodies to viruses to prevbent them from attaching to receptors
Opsinization
binding of antibodies to bacteria then macrophage can bind to the Fc or constant region of that antibody - increases phagocytosis
Agglutinization
Cross-linking of viruses and bacteria through at least bivalent antibodies to form clumps or aggregates
these clumps can be filtered out of the blood and lymph by the spleen and kidneys
Complement activaiton
the classic pathway of complement activation starts with antibodies binding to bacteria
MAC attack to punch holes through membranes
three ways for complement activation
Antibody dependent cell mediated cytotoxicity
works against large pathogens but also your own cells
antibodies bind to pathogen
NK cells and macrophages bind to the Fc or constant region of the antibodies and are stimulated to release granzymes to kill the pathogen
Two MHC classes
MHC I is found on all nucleated cells
MHC II is found only on macrophage, DC and B cells (aka APCs)
MHC protiens are found attached to the cell membrane but mostly outside the cell
All MHC protiens bind antigens and present them to receptors on other cells
MHC I proteins present antigens derived form inside the cell
these antigens are normally derived from host protiens so are “self” antigens
NK and CTL cells recognize these as “self” and do not attack those cells
When a cells is infected with a virus, or an intracellular bacteria “non-self” antigens are presented
NK and CTL cells recognize these as “non-self” and attack those cells and kill them (NK cells recognize the absence of MHC I)
MHC II protiens present antigens derived outside the cell
macrophage and DC phagocytoize antigens form outside the cell
antigens are broken up in phagolysosomes
parts of the antigens attack to MHC II and are displayed on the outside of antigen presenting cells
these interact with T cells to activate them
T cells
T cells produce a unique receptor TcR whihc is found on the surface of each T cell
also produced by random rearrangement of TcR genes
T cells are activated by binding Ag to the TcR
the antigen must be presented ot the T cell by another cell
Activation is achieved by binding of the TcR to the antigen attached tot he MHC molecule
macrophage and DC cells present using MHC II
all other cells present Ag using MHC I
Differentiation of T cells
T cells differentiate into T helper cells and CTLs
Th cells differentiate into Th1 and Th2 and Th17 cells
Th1 activate CTLs
Th2 activate B cells
CTLs when activated recognize virus and bacteria infected cells through MHC I and attack and kill them
which portion of the antibody does the NK cell bind to
Fc
antibody bind to cell, NK cell recognizes, and kills the antibody bound cell
Active immunity
creating your own immunity or activation of your own immune system because you actually got the infection
passive immunity
cells and antibodies that were created in somebody elses active immune response are transferred to you, you dont actually get the infection
convalescence plasma when no other better option is avalible
Herd immunity
not actually immunity, that is, not an individual immune response
in a population there are susceptible and non susceptible people
pathogens have to spread from host to host
if there are enough people in a population then the pathogen cannot find or spread to a new host// susceptible person
live attenuated vaccinces
a pathogen is weakened by a spontaneous process or by human intervention
live attenuated duck egg, serial passages to attapt to a non-human host to reduce virulence
cons, are recombination with wild types and attenuated vaccine can become virulent again
this pathogen is injected into people
in connot cause the disease but can replicate in the host
usually provides strong cell and humoral immunity often for life
inactivated vaccines
the pathogen is killed or made incapable of reproduction before being used in avaccine
phenols and propanol-lactones to inactivate viruses
not as strong an immune reaction and usually only humoral immunity is activated
subunit vaccines
contain only a single protein or several proteins from the pathogen
not as strong an immune reaction adn usually only humoral
ex= flu vaccines used today, H and N proteins only
toxoid vaccines
tetnus and diptheria vaccines
some bacterial infections are due solely to the production of a toxin
toxins are produced and inactivated and used in the vaccine via heat denaturation or gluteraldehyde
conjugate vaccines
polysaccharides are not immunogenic but are virulence factors (ie capsules)
bacterial polysaccharides are chemically bound// conjugated to protiens and used in a vaccinne
protein causes the production of Ab against the polysaccharide
DNA vaccines
the gene for an antigenic protien from the pathogen is inserted into a DNA plasmid moleucle
this plasmid is transfected into host cells
plasmid directs the transcription and translation of the pathogen protein
presentation of non-self protein on MHC I leads to immune system inactivaiton
mRNA vaccines
the gene for an antigenic protein from the pathogen is inserted into a DNA plasmid molecule
this plasmid is transfected into E. coli cells which are grown and lysed to obtain a lot of plasmid DNA
the plasmid DNA is used with enzymes 9RNA pol) to produce mRNA for the pathogen protein
how do we get the mRNA vaccine into you
the mRNA is packaged into lipid nanoparticles
these nanoparticles are injected into a person and the mRNA enters into the cytoplasm of the cell
cell translates the mRNA into protein which is presented as non=self protein on MHC I and leads to immune system inactivation
