Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/132

Click to flip

132 Cards in this Set

  • Front
  • Back
Ancient Egyptians, Indians, Chinese and Greeks observed life long immunity to what diseases?
Plague and small pox
Smallpox has a (low/high) mortality rate, and the survivors are scarred for life. Can survivors come down with small pox again?
High, never came down with it a 2nd time
During what time frame did Lady Mary Montagu convince the Royal College of Physicians in London to practice variolation?
1710's and 1720's
During what decades did several physicians draw attention to the fact that milkmaids exposed to cowpox develop protection against small pox?
1760's and 1770's
What did Jenner inoculate into the arm of young James Phipps?
Pustular fluid obtained from cowpox vesicles
Who had the first "immunological" experiment?

What was this experiment?

What type of vaccine did he administer to Joseph Meister?
Pasteur

He injected live bacillus from b. anthracis into control sheep and injected heat&chemically inactivated bacillus from b. anthracis into experimental sheep. The control sheep died. Experimental sheep that were given live bacillus afterwards were protected!

Rabies vaccine
Who was involved with the germline theory of disease?

He was the first to introduce the concept of what?
Robert Koch

First to introduce the concept of microbial origin of disease
What are Koch's 4 postulates?
1.The microorganism must be isolated from the diseased host and grown in pure culture.

2. The microorganism must be detectable in the infected host at every stage of the disease.

3. When susceptible, healthy animals are infected with pathogens from the pure culture, the specific symptoms of the disease must occur.

4. The microorganism must be re-isolated from the diseased/deceased animal and correspond to the original microorganism in pure culture.
Who discovered that WBC are phagocytic (engulf foreign particles)?
Elie Metchnikoff
What is Elvin Kabat famous for in the 1910-1950's?
Immunoglobulin
What are Karl Landsteiner and Merrill Chase famous for in the 1910-1950's?
Blood groups, antibody/antigen structure & interaction
Emil von Behring & Shibasaburo Kitasato (serum transfer provides immunity) and Elvin Kabat (immunoglobulin) advanced the study of (cellular/humoral) immunity.
Humoral
Elie Metchnikoff (WBC are phagocytic) and Karl Landsteiner & Merrill Chase (transfer of WBC contributes to immunity to M. tuberculosis in guinea pigs) advanced the study of (cellular/humoral) immunity.
Cellular
a) In what decade was the beginning of modern immunology?

b) Medawar, Owen, Billingham and Brent contributed to the study of what?

c) Ehrlich, Jerne, Talmage and Burnet contributed to what?
a) 1950's

b) Tolerance

c) Clonal Selection theory
T/F

Generation of diversity encompasses both germline and somatic mutation theory.
True!
In the 1950's to present, Jerne, Edelman, Milstein & Kohler, Zinkernagel & Doherty, Benacerraf, and Tonegawa have contributed to the study of what?
Cellular and molecular explanations of immunological events
What are the general pathogens encountered by our immune system?
Bacteria (prokaryotes)
Viruses (non-cellular)
Fungi (eukaryotes)
Parasites: protozoa (eu) and helminths (eu)
What is salmonella enteritidis?
a bacteria that causes food poisoning
What is mycobacterium tuberculosis?
a bacteria that causes tuberculosis
What is staphylococcus aureus?
a bacteria that is part of the normal flora of the skin, but can cause pimples and boils
What is pneumocystis carinii?
a fungus that causes pneumonia, especially in immunocompromised patients
What is candida albicans?
a fungus that causes thrush and systemic infection, especially in immunocompromised patients
What is epidermophyton floccosum?
a fungus that causes ringworm
What is schistosoma mansoni?
a parasite that causes schistosomiasis (has both males and females)
What is trypanosoma brucei?
a parasite that causes sleeping sickness
Which pathogen type is not a cell?
Virus
Which pathogen type is the smallest? the largest?
Smallest - virus (.02-.2 micrometer)

Largest - protozoa/helminth (15-25 micrometer)

Fungi - 3-10
Bacteria - 1-5
Which pathogen type has either RNA or DNA but NOT both?
Virus
Ribosomes are (70s/80s) for prokaryotes and (70s/80s) for eukaryotes.
70s, 80s
Which pathogen types have mitochondria?
Fungi, protozoa and helminths
Which pathogen type has a rigid wall with peptidoglycan?
Bacteria
Which pathogen has a rigid wall with chitin?
Fungi
Which pathogen has a flexible membrane for its outer surface?
Protozoa/helminths
Which pathogen has a protein capsid and lipid envelope?
Virus
Which pathogen types have motility?
Bacteria have some, and protozoa/helminths have a lot
Which pathogen type replicates by binary fission?
Bacteria
Which pathogen type replicates by budding/mitosis?
Fungi
Which pathogen type replicates by mitosis?
Protozoa/helminths
Which pathogen type has complex replication using host cell machinery?
Virus
Which entry routes into the body are mucosal surfaces?

What is the purpose of mucus?
airway, GI tract, reproductive tract

Mucus continually bathes mucosal surfaces, protecting the epithelial cells and limit infection.
a) What entry routes into the body consist of external epithelia?

b) What is the purpose of skin against pathogens?
a) External surface, wounds and abrasions, and insect bites

b) Skin forms a tough, impenetrable barrier of epithelium protected by layers of keratinized cells
How is influenza transmitted? (mode, route, organism)
Inhaled droplets/spores of influenza virus through the RT
How is meningococcal meningitis transmitted? (mode, route, organism)
Inhaled droplets/spores of Neisseria mengitidis through the RT
How is Typhoid fever transmitted? (mode, route, organism)
Water/food contaminated with Salmonella typhi through the GIT
How is rotaviurs transmitted and what disease does it cause? (mode, route)
Contaminated water/food through the GIT, causing diarrhea
How is Syphillis transmitted? (mode, route, organism)
Physical contact with Treponema pallidum through the reproductive tract.
How is AIDS transmitted? (mode, route, organism)
Physical contact with HIV through the reproductive tract.
How is Athlete's foot transmitted? (mode, route, organism)
Physical contact with Trichophyton through the external surface.
How is cutaneous anthrax transmitted? (mode, route, organism)
Skin abrasions with Bacillus anthracis
How is Tetanus transmitted (mode, route, organism)
Puncture wounds with Clostridium tetani
How is Tularemia transmitted? (mode, route, organism)
Animal handling with Francisella tularensis through wounds & abrasions
How is Yellow fever transmitted? (mode, route, organism)
Mosquito bites (aedes aegypt) with Flavivirus
How is Lyme disease transmitted? (mode, route, organism)
Deer tick bites with Borrelia burgdorferi
How is Malaria transmitted? (mode, route, organism)
Mosquito bites (anopheles) with Plasmodium spp.
T/F

Adaptive immune response occurs as soon as the innate immune response.
False!

There is a threshold level of antigen/microorganism to activate the adaptive immune response
What 2 things does the clearance of pathogens depend on?
1. Prompt microbial recognition by a group of cells called antigen presenting cells (Dendritic cells, macrophages, and B cells)

2. Efficient function of the effector cells which destroy and eliminate the pathogens (neutrophils, macrophages, NK cells, and effector T and B cells)
Epithelial cells joined by tight junctions, such as keratinized skin, which is waterproof and renews completely every 15-30 days, is an example of a (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?
Mechanical

Skin, gut, lungs, eyes/nose
Longitudinal flow of air or fluid is an example of a (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?
Mechanical

Skin and gut
Movement of mucus by cilia is an example of a (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?
Mechanical

Lungs
Lactic acid, fatty acids, and low pH are an example of a (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?
Chemical

Skin
Low pH and enzymes such as pepsin are examples of a (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?
Chemical

Gut
Surfactants A & D are examples of a (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?
Chemical

Lungs
How do Surfactants A & D protect against pathogens?
They function as opsonins, which enhance the efficiency of phagocytosis
Salivary enzymes, such as lysozyme, are an example of a (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?
Chemical

Eyes/nose
How does lysozyme protect against pathogens?
It is a hydrolytic enzyme and cleaves the peptidoglycan layer of the bacterial cell wall
Antibacterial peptides (defensins) are an example of a (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?
Chemical

Skin, gut and lungs
How do antibacterial peptides (defensins) protect against pathogens?

a) Where is alpha-defensin made?
b) Where is beta-defensin made?
Defensins kill bacteria, fungus and enveloped viruses by perturbing their membrane.

a) cryptidine made by paneth cells of the small intestine

b) epithelial cells of the epidermis, GI and respiratory tract
Normal flora is an example of a (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?
Microbiological

Skin and gut
How does normal flora defend against pathogens?
It competes with them for nutrients and attachment sites on epithelial cells
What are some examples of normal flora?
S. aureus, S. epidermidis, Streptococcus species, Propionibacterium, E. coli, etc.
What on the cell surface of innate immunity cells, such as macrophages, is responsible for recognizing pathogens in the innate immune response? What is the name for them?
A group of germline encoded receptors of several different structural types, that can bind to a diverse array of ligands including peptide, proteins, glycoproteins, peptidoglycan, carbohydrate, glycolipids, phospholipids, and nucleic acids.
They are called Pattern Recognition Receptors (PRR)
Germline encoded receptors (PPR) on the cell surface of innate immunity cells (such as macrophages) recognize a specific pattern or molecular signature of a particular group or organism. What is this called?
Pathogen associated molecular pattern (PAMP)
Mannose receptors are specific for what?
Fungi
LPS receptors and Toll (TLR4?) receptors are specific for what?
Gram negative bacteria
Inflammation is a coordinated response to cell injury characterized by what 5 things?
Heat (calor), pain (dolor), redness (rubor), swelling (tumor) and sometimes loss of function
What induces inflammation?
A variety of inflammatory mediators released as a consequence of pathogen recognition by macrophages - cytokines, complements, PGs, leukotriens, and platelet activating factor.
What do inflammatory mediators (cytokines, complements, PGs, leukotriens, platelet activating factor) all function together to do?
1. Deliver effector molecules and cells to site of infection to augment destruction of invading organisms by tissue macrophages

2. Provide physical barrier to prevent spread of infection

3. Promote repair
What is released by injured tissue? What is activated?
Releases cytokines, chemokines, and other mediators. Activates complements.
What induces dilation of blood capillaries in inflammation?

What does this cause?
Cytokines

This causes increases blood flow, making the area red and warm
What increases cell recruitment (neutrophil, macrophage) to the site of injury?

How?
Cytokines and chemokines

By upregulated adhesion molecule expression on the endothelium.

These cells present at the site of inflammation are called inflammatory cells
What happens when vasodilation induces gaps between the endothelial cells?
There is increased leak of blood plasma into the interstitial cells, causing a local increase in fluid volume -> edema or swelling
What causes the pain during inflammation?
The increase in fluid volume puts pressure on nerve endings. PG, one of the inflammatory mediators, is also a potent pain inducer!
T/F

It benefits the host that inflammation calls upon a delayed engagement of the host-immune response.
False!

inflammation calls upon an immediate engagement of the host-immune response, and in most of the cases contain the infection.
In the innate immune response, macrophages engulf the pathogen and produce what?
Cytokines and chemokines, which, along with other inflammatory mediators, induce a local inflammatory response.
Why does the innate immune response recruits neutrophils and NK cells to the site of infection?
To enhance the immune response
What is the function of complements in the innate immune response?
They act as a molecular tag and enhance the performance of effector cells, and they also form protein complexes to damage the pathogen cell membrane (membrane attack complex).
Innate immunity is (fixed/adaptive) and adaptive immunity is (fixed/adaptive).
Fixed, adaptive
Innate immunity is (slow to develop/immediate) and adaptive immunity is (slow to develop/immediate).
Immediate, slow to develop
Innate immunity is (specific/non-specific) and adaptive immunity is (specific/non-specific).
Non-specific, specific
Innate immunity (does/does not) have immunological memory, and adaptive immunity (does/does not) have immunological memory.
Does not, does
Innate immunity (does/does not) have self and non-self discrimination, and adaptive immunity (does/does not) have self and non-self discrimination.
Does, does

Both do, but innate is not as developed as adaptive. Adaptive is responsible for rejection of skin or organ graft from donor of the same species.
Which is more diverse - innate or adaptive immunity?
Adaptive
What happens if the innate immune response fails?
Adaptive immune response takes over
Antigenic component receptors on (T/B) cells undergo somatic hypermutation.
B cells
Ig on B cells or T cell receptor (TCR) on T cells recognize and bind molecules, macromolecules, virus particles or cell that contains a structure specific for them. What are these collectively called?
Antigen
What is the particular part of the antigen bound by the Ig or TCR called?
Antigenic determinant or epitope
T/F

The interaction between antigen and Ig or TCR is specific.
False!

The interaction is specific!
a) Ig is formed by (#) different polypeptides. What kinds of chains are these?

b) Which region of Ig is at the amino terminus and contains the antigen binding site?

c) Which region has a binding site for cell-surface receptors on phagocytes, inflammatory cells, and complement proteins?
a) 2, heavy and light chains

b) Variable region

c) Constant region
What are the 5 different Ig isotopes? What are their differences based on?
IgM, IgD, IgG, IgA, IgE

On the basis of different constant regions

Cell surface IgM and IgD are the Ag receptors.
Antibodies are secreted Ig's, lacking what region?
Transmembrane region
How many chains are in a TCR? What are the types?
2, alpha and beta chains

(both anchored in T cell membrane, both have a variable and a constant region, variable region has antigen binding site)
What determines the availability of a pathogen-specific receptor on a lymphocyte?
It is genetically determined and occurs at random
T/F

Selection of a receptor on lymphocytes by a pathoen depends on the availability of the receptor specific for that pathogen.
True!
T/F

Receptors on lymphocytes are germline encoded.
True!

They subsequently undergo certain genetic rearrangements, giving rise to millions of diverse receptors specific for all possible pathogens.
T/F

Each lymphocyte cell carries multiple types of receptors specific for several Ags.
False!

Each cell carries 1 type of receptor specific for any particular Ag
When are effector cells produced and what do they do?
Proliferation and differentiation of lymphocytes (after encounter of a lymphocyte receptor with a specific Ag), produces a clone of effector cells (clonal selection).

Effector cells are equipped with the ability to kill pathogens, directly or indirectly.
What is the key principle for developing a diverse but specific adaptive immune system?
Clonal selection
Rearrangement of different gene segments of Ig and TCR in the soma is called what?
Somatic recombination
What are the different ways that diversity is created between Igs and TCRs?
- rearrangement of germline DNA segments
- rearrangement of different gene segments of Ig and TCR in soma (somatic recombination)
- various alternative forms of genes encoding the variable regions can rearrange in numerous different combinations
- various combination of light and heavy chains in Ig molecules
- addition of new nucleotides at the junction of V region gene segments result in additional diversity of hypervariable region -> called junctional diversity!
ONLY FOR Ig

After encounter with pathogen, activated B cells in the secondary lymphoid tissue undergo a process which involves nucleotide substitution into the Ig heavy and light chain genes. What is this process called?

Some of the variant mutant Ig produced in this process bing the antigen strongly and become Ab-secreting plasma cells. What is this process called?
Somatic hypermutation

Affinity maturation
T/F

Abs bind to intact components of the pathogen surface, such as glycoprotein or proteoglycan.
True!
T/F

The epitope can be carbohydrate groups, clusters of amino acid, or combinations of the two.
True!
a) (TCR/Ig) binds only short peptides presented to them in the form of a complex with a membrane glycoprotein called what?

b) What are these short peptides derived from?
a) TCR, major histocompatibility complex (MHC)

b) derived from the breakdown of the pathogen molecule within the cell expressing the MHC molecules
Cells that present peptides to the TCR are called what?
Antigen-presenting cells
Viruses or certain intracellular bacteria that reside in the cytosolic vesicles of the infected cell and use the cellular machinery for multiplication are bound to WHAT in the ER (after being degraded to smaller peptide fragments)?
MHC class 1 molecule
Peptide fragments (of viruses or intracellular bacteria) bound to MHC 1 are transported to the cell surface to be recognized by what type of cell? What then happens?
CD8 T cells (cytotoxic T cells)

They will kill the virus-infected cell!
Peptide fragments bound to MHC 2 are transported to the cell surface and recognized by what type of cell? What then happens?
CD4 T cells (helper T (TH) cells)

They will interact with APC and will augment their functions
(B cells/macrophages) interact with TH1 cells, while (B cells/macrophages) interact with TH2 cells.
Macrophages -> TH1

B cells -> TH2
What is the term for when an antibody binds intact pathogen and toxins and neutralizes their function by inhibiting microbial growth, replication, or interaction with human cells?
Neutralization
What is it the term for when IgG coats the surface of extracellular pathogens and toxins and then facilitates their engulfment by phagocytes, which carry specific receptors for the constant region of Ab molecules?
Opsonization
When the Ab involved is an IgG, opsonization occurs in two ways.
But, when the Ab involved is an IgM, what is the only mechanism for opsonization? Why?
Opsonization by complement activation, because phagocytes do not have a receptor for IgM constant region
Thymocytes with different TCR interact with MHCI and MHCII molecules on cortical epithelia.

a) Cells that interact strongly are saved, while others are discarded. What is this process called?

b) Cells that bind TOO strongly with MHC molecules are signaled to die by apoptosis -> therefore, generated T cells are self-tolerant. What is this process called?
a) Positive selection

b) Negative selection
What happens to clones of B cells with Ig receptors that bind strongly to bone marrow constituent cells?
Eliminated by induction of apoptosis
How does the secondary response of antibody and effector T cells to an infection compare to the primary response in duration and intensity?
The secondary response occurs in much shorter time with a significantly greater intensity.

*This principle underlies the success of vaccinations
(TH1/TH2) cells induce B cell differentiation to plasma cells. (TH1/TH2) cells, differentiated in response to specific Ag stimulation, activate macrophages for effector killing function.
TH2, TH1
What do cytotoxic T cells (CTL) do?
Kill virally infected cells
What happens when you lack innate immunity?
Uncontrolled infection, as adaptive immunity can not be deployed without preceding innate response
What happens when you lack adaptive immunity?
Initially controlled by innate immunity, but it will fail to clear eventually
What is the term for a clinical condition where the host immune system responds to inocuous substances in the environment, usually as a secondary response when re-exposure to an Ag causes the Ag to bind to an IgE Ab (formed from previous exposure and bound to receptors on mast cells via constant region)?
Allergy or hypersensitivity
Degranulation of mast cells, releasing histamine, cytokines, leukotriens, bradykinins, and others, caused by allergic reaction, are mediators that may give rise to severe life threatening conditions such as what?
Acute bronchial asthma and systemic anaphylaxis
Development of insulin-dependent diabetes mellitus (IDDM) has been correlated with previous infection with what?
Coxsackie virus
Why do symptoms appear later in IDDM?
Healthy pancreas can make much more insulin than required, so symptoms occur later when substantial numbers of pancreatic beta cells have been destroyed by virus specific CTLs, which is also specific for peptide. MHC complex is expressed on beta cells.