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3 characteristics of the immune system:

1. Specificity a response able to contain one pathogen is unlikely to work for a

different one.
2. Universality the immune system is able to respond to all types of
3. Adaptability the immune system can adapt, i.e. immune responses takes
time to develop in response to a pathogen, i.e. secondary responses
positive/negative memory.
Innate resistance present all the time, dont change due to infection.
3 defence mechanisms in vertebrates are skin, innate defense by cells, and the
immune system.
Innate defense by cells:

Inflammation via histamine released by mast cells at the skin.

Macrophage bind to bacteria = phagosome, which fuses with a lysozyme =
o Complement component C3b, binds to bacteria, easier for
macrophage binding.
Complement cascades via complement components (e.g. lysis of bacteria)
Interferon production
o Cell infected with a virus releases interferons, which are taken up by
nearby uninfected cells produce antiviral proteins.

Attenuate/make weaker bacteria by exposing to anaerobic conditions or high temps,

or by passing the virus through another other animal species.
Salk vaccine = dead virus. Sabin vaccine = attenuated virus.
Exotoxin poison shed from pathogen.
no longer toxic.

Toxoid toxin treated so that its

Immune serum cell-free yellow liquid that separates from clotted blood of an
immunized animal.

Contains antibodies; antibodies act as adaptors for others to attack the

antigen. E.g. Opsonin
Giving immune serum to an unimmunized animal gives passive immunity.
Precipitin reaction = precipitate formed from antibody + antigen binding.
Heated immune serum contains only ABs, non-heated serum contains
complement components for bacterial cell lysis.

Humoral Immunity make antibodies transferrable

Cell-mediated immunity requires transfer of cells for immunity to pass on better
at containing mycobacterium
After immunization, injecting an antigen into the skin can cause either Immediatetype hypersensitivity, or delayed-type hypersensitivity.

Self-nonself discrimination ability to tell your cells and foreign cells apart.
Allergies are due to the induction of IgE antibodies
Antibodies are made of one basic unit: 2 light and 2 dark chains,

light chains have 2 parts, first 110aa=constant region, last 110aa=variable

dark chains have 5 parts, first domain is variable, other domains determine
antibody class
o IgM, IgA, IgE, IgM constant domains are identical in heavy chains of
ABs of same class.
o IgG & IgE = 1 basic unit, IgA >1 basic unit, IgM = 5 basic units.

Antibodies and antigens bind together to form lattice = Precipitin reaction.

Cells that respond to antigens are clonal (from a precursor cell), they are selected
for by the antigen.
Self-antigens (self-molecules) present early in development = self-nonself
Major Histocompatibility complex (MHC) molecules digest intracellular proteins,
display on membrane:

Class 1 found on surface of all cells in the body if the cell start presenting
proteins on the membrane that shouldnt be there, signal sent to immune
system to fix.
Class 2 found on surface of phagocytic cells shows what antigen it just

B cells are made in Bone Marrow, stored in lymphoid organs (e.g. Spleen and Lymph
T cells made in the Thymus, do not bind to antigen itself, but to antigens displayed
on MHC molecules.

T cells are antigen specific, there are no T cells for self-antigens.

CD4+ T cells bind peptides displayed by class 2 MHC molecules
CD8+ T cells bind peptides displayed by class 1 MHC molecules.

Immunogenic molecules that induce antibody production (conversely

nonimmunogenic is opposite).
Hapten nonimmunogenic alone, but when conjugated w/ an immunogenic
molecule = hapten-conjugate complex = a whole different immunogenic molecule.

The Hapten alone can bind to the antibodies produced for the haptenconjugate complex; the conjugate however cannot.

Antigen binding to precursor cell itself does not induce Antibody production, needs
helper T cell.

Helper T cells only exist for foreign antigens, not self-antibodies.

B cell + antigen + Helper T cell = antigen bridge model.

Antigen-specific inactivation: B cell receptors bind to self-antigens

death of B cell
Epitope complementary part between antigen and antibody.

If 2 molecules have epitopes in common = crossreact; similar antigens can

induce B-cells in different organism systems.
Hashimotos disease autoimmune disease to the thyroid have
antibodies in their immune serum that react with thyroglobulin.
Group A streptococci crossreacts with heart tissue

Cell mediated responses best for mycobacterium infections, antibodies best to

neutralize toxins.

Induction of 1 response inhibits the other response

2 types CD4+ T cells; when stimulated by Class 2 MHC of phagocytes w/antigen, will
secrete cytokines:

Th1 cells produce IL2 (growth factor for all T cells) and IFNg (interferon
prevent viral multiplication, and it is used for macrophage activation)
o IFNg and IL2 cytokines promote cell mediated immunity.
Th2 cells produce IL4 (inhibits cell-mediated immunity) and IL10
cytokines, which promote humoral immunity.

Future treatment:

Some people never become allergic because they produce IgE instead of IgG
in response to allergen.
B7 molecules on macrophages and CD28 molecules on CD4+ T cells allow
them to bind together.
Having B7 molecules on cancer cells easier to stimulate T cells.