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What is the difference between innate immunity, and acquired immunity?

Innate immunity-Non-specific
Acquired immunity-Specific

Nonspecific resistance( Innate Immunity)

-Physical barriers
-Chemical barriers
-Cellular defenses-phagocytes & phagocytosis
-Molecular defenses:Interferon, complement

Specific resistance(Acquired Immunity)

-AB(antibody) mediated(humoral) immunity
-Cellular Immunity


A substance the body recognizes as FOREIGN and to which it mounts IMMUNE response
-Immunogenic: Stimulates an immune response(immunogen)
-Reactive: reacts w/ immune response
-Large complex molecules

Composed of many antigenic determinants(epitopes)

-The part of the Ag that actually stimulates & reacts with the immune response

Antigens based on?

Diversity of structure
How long is stays in the body
-Some molecules are too small to be antigens


A molecule that by itself is too small to be immunogenic
-Is immunogenic when attached to a larger molcule

Key cells are?


B lymphocytes

-Arise in bone marrow
-Primarily involved in antibody-mediated immunity

T lymphocytes

-Arise in the thymus gland
-Primarily involved in cell-mediated immunity

Do B-cells and T-cells have different receptors?

yes, each have an antibody molecule that recognizes and binds to a specific Ag

General Properties of Immune responses(Recognition of self vs non-self)

-Self=host tissue
-non-self=all foreign substances
Tolerance=The host doesn't mount an immune response to "self" Ags, under normal circumstances(tolerant)

General properties of Immune responses(specificity)

-Each immune reaction if directed toward a specific Ag
-The response to 1 Ag doesn't affect the response to another
-Yet, cross-reactions can occur if 2 Ags are similar(share Epitopes)

General properties of Immune responses(Diversity)

-The immune system can respond to many different Ags( >1billion)

General properties of immune responses(Memory)

-The immune system can recognize Ags it has previously encountered
-It responds more quickly the second/subsequent time it encounters that Ag

Antibodies(Ab) are

-Proteins that circulate in the bloodstream
-Immunoglobins-Immune, globins(antibody factories)
-Synthesized and secreted by plasma cells
-B lymphocytes that circulate in the bloodstream and synthesize & secrete Ab
-Each Ab is specific for 1 particular antigenic determinant
-React w/ Ag that is outside host cell; Ex: toxins, viruses

Development of Ab response(Ags enter Lymphatic tissue and encounter B cells)

-B cells have specific Ab on surface
-Ag & Ab interact, activating the B cell

Development of Ab response(Activated B cells interact with T helper cells)

-Helper T cells secrete cytokines, which further activate B cells
-B cells differentiate into
-Plasma cells-Ab-producing cells in the blood stream
-B memory cells- remain in tissues, responsible for immunologic memory.


Cell communication molecule; released by one cell to signal another.

Structure of Ab molecule

-4 Polypeptide chains-2 heavy, 2 light
-Ag-binding site: Each Ab molecule can bind 2 Ag molecules(Ag-Ab complexes)
-Complement-activating(binding) site
-Binding to macrophage-Ab are opsonic
-Cell-binding site; Each Ab molecules has a cell binding site
-Binding to B cells, as a surface receptor

Immunoglobulin( IgM)

-A pentamer
- First to appear. especially in primary Ab responses
-In bloodstream: on surface of B cells

Immunoglobulin( IgG)

A monomer
-The major circulating Ab,
Appears later than IgM, especially in secondary Ab responses
Crosses placenta

Immunoglobulin( IgA)

A monomer or dimer
-occurs in Serum(monomer) and in Secretions(dimer); secreted onto mucosal surfaces, in tears, saliva, & colostrum.

Immunoglobulin( IgE)

A monomer
-on surface of mast cells and plays a role in Allergic reactions

Immunoglobulin( IgD)

A monomer
-Surface receptor on B lymphocytes

Primary Ab response

-Occurs first time an Ag is encountered
-Ab begins to appear in ~5days
-First Ab is IgM, then it wanes
-Next Ab is IgG, appears in greater amount

Secondary Ab response

-Occurs at second/subsequent Ag exposure
-Results from B memory cells
-Occurs more quickly than primary response
-Produces more Ab then primary response
-Last longer then primary response

What will happen at the 3rd Ag response?

Same as 2nd Ag response

What is a booster shot?

A trigger to get a secondary response

Why are some vaccines given as a series of shots?

To ensure a secondary Ab response results

Why do we have a secondary response

Because there is more Ab
-Last longer than primary response

If you find a specific Ab to a pathogen in serum, what does that mean?

Either present infection, or previous exposure

How could you use Ab to diagnose infections?

Look for IgM-for current infection
-Compare Titer in acute & convalescent sera (titer=amount of Ab)

Can an antibody kill a microbe all by itself?

No, it needs help

How do antibodies work?(neutralize viruses)

Prevent them from entering/infecting cells

How do antibodies work?(neutralizing viruses)

Prevent them from binding to receptor to affect host

How do antibodies work?(Block adhesion)

Bind adhesion, prevent from attaching and colonizing host

How do antibodies work?(Opsonize)

enhance phagocytosis
-Ab is an opsonin, a handle for phagocytosis

How do antibodies work?(agglutinate)

Clump particles together, making them easier to phagocytose

How do antibodies work?(precipitate)

Clump soluble molecules together, making them easier to phagocyose

How do antibodies work?(Activate complement)

Forms MAC(memory attack complex) resulting in Lysis, killing of pathogens

Antibody mediated immunity
-Depends primarily on?
-More active against?

-B cells & Ab
-Extracellular, microbes and molecules

Cell mediated immunity
-Depends primarily on?
-More active against?

-T cells & their direct action against microbes
-Infected cells, Cancer cells, Transplanted cells

Main cell types in Cell-mediated immunity(Antigen-presenting cells)

-Usually macrophages
-Function; Find, process & present Ag to T-cells

Main cells type in Cell-mediated immunity(Cytotoxic T cells)

-CD8 corecptor on surface
-Function: kill & lyse target cells that display their particular Ag

Main cell type in cell-mediated immunity(Helper T-cells)

CD4 coreceptors on surface
-Function: help in development of Ab or a cell-mediated immune response

Main cell types in cell-mediated immunity(memory T cells)

-Function: provide memory response; respond quickly with subsequent exposure

Development of cell-mediated Immune response

1. Ag is recognized and phagocytosed by macrophages-Antigen-presenting cells
2.Macrophages finds corresponding helper T cell: presents Ag(binds)
3.Helper T cell becomes activated
-Cytokines-cell communication molecules; released by one cell to sign or stimulate another cell (ex: interluekin)
4.Helper T cell starts dividing, expanding into a clone of help T cells
5.Ag-presenting cells also activate cytotxic T cells to divide
6.Cytotoxic T cells binds & destroys target cell.
PEFORINS-Released from cytotoxic T cells: forms pores in target cell memebranes

Why does HIV infection result in immunodeficiency

-Infects Helper T cells; Its receptor is CD4
-Helper T cells are destroyed, host can't develop Immune response

Why is it so difficult to make a vaccine for HIV/Aids?

-The virus destroys a hosts ability to make an immune response

Types of acquired immunity(passive vs active)

Passive-Immune response provided to the host
Active-Immune response develops within the host

Types of acquired immunity(natural vs artificial)

Natural-Immune response develops naturally
-Artificial-Immune response develops after an intentional or purposeful action

What is natural,active immunity?

-exposure to infectious agent, or occurrence of infection -Clinical or subclinical disease can trigger immune response

What is Artificial,active immunity

Ex: immunization, vaccine

What is natural, passive immunity

-Maternal Ab provided to fetus/newborn
-Ab crosses the placenta( protects for 3-6 months)
-Ab in colostrum & breast milk, protects G.I. tract

What is Artificial, passive Immunity

-Administration of preforms Ab to a host
-Antiserum, hyperimmune serum, immune globulin, or gamma-globulin
This is done:Botulism antitoxin,Antivenon,Tetanus immune globulin, Rabies immune globulin.

Active, passive immunity
How quick is the host immune?
How long does it last?

-Ab might be seen as foreign-can cause Serum Sickness(an allergic reaction)

Inactivated vaccine

-Whole bacterium or virus is killed and administered as an Ag
Ex: Influenza vaccine, inactivated polio virus
Advantage? No danger of getting disease from vaccine
Concern? Side affects, due to extraneous microbial components

Attenuated Vaccine

Live vaccine with reduced pathogenicity, is administered, causing a small subclinical infection
Advantage? Longer-lasting immunity than inactivated vaccine
Concerns?Reverse to virulence
Immuno-surpressed patient

Subunit Vaccine

Only 1 subunit or part of an organism is the Ag, not the whole organism
Advantage?Clean, fewer side effects


Inactive toxin is given as Ag: has lost its toxic activity but retained its immunogenicity
ex: tetanus, botulism vaccines

Conjugate vaccine

A subunit is linked or conjugated to another molecule to increase its immunogenicity


a conjugate vaccine, capsular polysaccharide conjugated to diptheria toxoid.

Syntheitc vaccine/ recombinant vaccine

a Subunit or part of an organism is produced using genetic engineering
ex:Hep b virus-hep B surface Ag is produced in yeast cells

Advantage of Synthetic vaccine

Ease of production
No danger of whole virus contamination
lower side effects

Does everyone in a population need to be vaccinated to be protected from disease?

yes, at an individual level
no, at a population level

Herd immunity

90-90% of population vaccinated
difficult for a disease to spread in the population in a sufficient number of individuals immunized.

What happens if % of people vaccinated in population drops below herd numbers?

Herd immunity breaks down, disease re-enters.

Adverse reactions to vaccines

Soreness at injections(non-specific defenses)
Hypersensitivity or allergy to vaccine components
Reaction to preservative-thimersol(mercury)


Measles, Mumps, Rubella,-a very effect vaccine


Highly communicable disease
Enveloped, ssRNA(- strand) with spikes
Red, macupapular rash that fades after ~1 week
Measles vaccine-1963


Is spread my respiratory droplets
Systemic virus infection with painful swelling of the parotid(salivary) glands
possible complication with young adult males-orchitis(testes inflmmation)
mumps vaccine 1967

Rubella(german measles)

as an acute but mildly infectious disease
red maculopapular rash begining on face and spreading to the body and extremities
risk of spreading to fetus
Rubella vaccine 1969

Hepatitis B vaccine-the first recombination vaccine

HepB can be acute or chronic
an enveloped, icosahedral, dsDNA virus in the depadnaviridae
Hepatitis B surface Ag is a viral envelope protein
-produced in excess and circulates in the blood stream

Hepatitis B effects

transmitted by contact with blood or body fluids of infected person.
Virus infects liver, cytotoxic T cells destroy virus-infected liver cells->liver damage->liver failure
a few develop hepatic cancer

Acute&chronic infection of Hep B

Acute-Asymptomatic to fever, fatigue,abdominal pain, jaundice
Chronic-Host is a carrier of the virus
Chronic-Antivirals(including interferon) and monitor liver

Hep B vaccine

a recombination vaccine
-HepB surface Ag produced in yeast cells
-95% effective in preventing hepatitis B
-Recommended for health care workers
-Became available in 1986


Transmitted by skin contact
30% fatality rate
Serious skin disease: macules->papules->vesicles->pustules->pocks(scars)

Smallpox vaccine

Administered by scraping/poking attenuated virus into skin of the upper arm, stopped in 1972.
Was purposefully spread in years was less variolation

Smallpox bio terrorism

Vaccinations have stopped worlwide; many people have immunity, immunity is waning in vaccines
-aerosal dispersal of virus could infect lerge number
highly transmissible


An increased,exaggerated, or inappropriate immune response that negatively affects the host. too much of a good thing.
A host is senstized, if they are hypersensitive to a particular Ag.
Sensitizing dose-1st exposure, proactive dose-2nd or later

4 types of hypersensitivity

type 1(immediate-type hypersensitivity)
type 2(Cytotoxic hypersensitivity)
type 3(Immune complex hypersensitivity)
type 4(Cell-mediated hypersensitivity)

Type 1(immediate type)

IgE that binds to surface
involved mast cells, and basophils
-Wheal and flare-skin reaction characterized by a swollen white center surrounded by redness, itching
happens in secs-mins

Histamine works by

Dilates capillaries
increases vascular permeability
constricts smooth muscle
increases mucus secretion
stimulates nerve endings->itch or pain

asthma/systemic anaphylaxis

asthma-occurs in the lower respiratory tract
systemic anaphylaxis-Ag in the bloodstream
-Can be rapidly fatal(~15 mins)
ex: bee stings, drugs
Treatment: Epi-pen(epinephrine)-inhibits degranulation, constricts blood vessels, relaxes smooth muscles.

How do we control Type 1 hypersensitivities

Avoid contact with allergen
Prophylactic antihistamine

How to fix/cure Type 1

repeated injections of small amounts of denatured Ag
May prevent B cells from maturing into IgE-secreting plasma cells
May induce tolerance to the Ag

Blocking Ab in type 1

Immunizing with the denatured allergen to produce serum IgG
Serum IgG "blocks" allergen from reaching Ig

What is allergen testing

poking with allergens, looking for reactions

What are allergy shots

Once a week, then eventually once a month, 50% rate works
Build up desensitization

Why are allergy and asthma rates increasing

States that lack of early childhood exposure to Ags & infectious agents leads to a weakened immune system and predisposes to allergies/asthma

Type 2 cytotoxic hypersensitivity

Ab-usually IgG or IgM
Ag- on the surface of cells
-Timing: adverse effects appear within min-hours

Transfusion reaction( Type 2)

ABO bllod groups-A,B,AB,O
Polysaccharide Ag on rbc surface
Ab in serum to the Ags you don't have
Your Ab will destroy incompatible rbc
Anemia, with clogged circulation & kidneys

Persons with what blood type are at greatest risk for transfusion reaction?

O-antibodies to both types

Persons with what blood type are at least risk for transfusion reaction?

AB- no antibodies

What happens when Rh-neg woman marries Rh-pos man and has a child?

First prego-nothing-woman builds Rh antigen ab

Subsequent prego-Anti-Rh antibodies enter fetal circulation, fetal rbc's destroyed

Treatment of Hemolytic disease of the newborn

Rhogam: rh AB-artificial passive
administered at birth of first Rh+ child
Binds up Rh Ag, preventing it from stimulating mothers immune system
So that anti-Rh Ab is not produced

Type 3 immune complex hypersensitivity

Ags-usually soluble; usually large amount entering the host
Abs-IgM or IgG
Timing: adverse effects appear within hours-days

Serum sickness(type 3)-sensitized

Ab develops to Ags in an antiserum preparation
Next administration: Ag-Ab complexes form and damage kidneys

Arthus reaction(type 3)

Immune complex formation where large amounts of Ag is entering the body.
Ex: farmers lung-Ag's in moldy hay

Type 4 cell-mediated hypersensitivity

Ags-usually displayed on cells or have become attached to cell surfaces
Sensitized T cells
-Generated upon first exposure to Ag
-React on second exposure to Ag
Often observed as a skin reaction
Timing: Delayed; starts after more than 12 hours up to week

Contact dermatitis(type 4)

CMI response develops to Ag deposited on the skin
Poison ivy
Other contact allergens

Tuberculin sensitivity-Tb test

CMI response develops from infection
tuberculin skin test provides second exposure to Ag
Positive test occurs-raised skin
Positive test-means exposure, not that you have it

Granulomatous hypersensitivity

Macrophages have phagocytosed pathogens but can't kill them
Sensitized T cells respond to form a granuloma

Autoimmune disorders(autoimmunity)

Hosts mounts immune response against its OWN ag's, cells, or tissues
-Host should be TOLERANT to self
-a good thing turned bad
reaction typically results in the destruction of host cells or tissues


The self Ag to which the host is responding.
Immune response may involve AutoAB, or may involved cellular response

How does Immunity to self develop?

Antigenic mimicry->cross-reactions between a foreign and self antigen
Tolerance failed to develop-cells that respond to "self" Ags were not destroyed in development of the immune system
-immune response to lens of the eye
-genetic factor

Myasthenia gravis( autoimmune disorder)

-affects skeletal muscles; unable to contract properly
-AutoAb against neurotransmitter receptor at nerve-muscle junction

Rheumatoid arthritis

AutoAg unclear (possibly nuclear Ags)
Immune complexes from in the joints

Systemic lupus erythromatosus

Ab to nuclear components of host's cells
Immune complexes form in the skin, organs

Immunodeficiency diseases

Immune system responds inadequately to an Ag, due to a genetic or acquired defect defect in the immune system
Too little of a good thing

Primary immunodeficiency

Genetic or developmental defect in immunity

Secondary immunodeficiency

Results from damage to immune cells after they have developed normally
Ex: HIV,cancer,leukemia

what will be the effect or appearance of immunodeficiency

Sick all the time

What would you expect if B lymphocytes failed to develop in bone marrow

Antibodies,plasma cells, b cells would be missing, it would show after 6-12 months due to breastfeeding

how to treat failed development of B lymphocytes

Bone marrow transplant, no vaccines


Sever combined immunodeficiency
Occures when stem cells in bone marrow don't develop into B,T cells (whole immune system missing)
Treatment: Bone marrow transplant, Possible gene therapy.

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