S2 I&i Exam 4: Intro To Immunology

Front 1

Ancient Egyptians, Indians, Chinese and Greeks observed life long immunity to what diseases?

Back 1

Plague and small pox

Front 2

Smallpox has a (low/high) mortality rate, and the survivors are scarred for life. Can survivors come down with small pox again?

Back 2

High

never came down with it a 2nd time

Front 3

When did Lady Mary Montagu (saw practice in India, injected own son) convince the Royal College of Physicians in London to practice variolation?

Back 3

1710's and 1720's

Front 4

By what decades had several physicians recognized that milkmaids exposed to cowpox develop protection against small pox?

Back 4

1760's and 1770's

Front 5

(May 14, 1796)
What did Jenner inoculate into the arm of young James Phipps?

Back 5

Pustular fluid obtained from cowpox vesicles


(then injected w/ small pox & boy survived)

Front 6

(1880-1910)
Who had the first "immunological" experiment?

What was this experiment?

What type of vaccine did he administer to Joseph Meister (infected prior to vaccination)?

Back 6

Pasteur

1. He injected live heat&chemically inactivated bacillus from b. anthracis into experimental sheep.
2. Then he injected experimental sheep & control sheep w/ live bacillus.
3. Control sheep died & experimental group lived

Rabies vaccine (from spinal tap of rabies animal)

Front 7

(1880-1910)
Who was involved with the germline theory of disease?

He was the first to introduce the concept of what?

Back 7

Robert Koch

First to introduce the concept of microbial origin of disease

Front 8

What are Koch's 4 postulates?

Back 8

1. microorganism must be able to be isolated from diseased host & grown in pure culture.

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

3. If susceptible, healthy animals are infected w/ pathogens from culture, specific symptoms must occur.

4. microorganism must be able to be re-isolated from newly diseased animal & match original

Front 9

(1880-1910)
Who discovered that WBC are phagocytic (engulf foreign particles)?

Back 9

Elie Metchnikoff

Front 10

What is Elvin Kabat famous for in the 1910-1950's?

Back 10

Immunoglobulin

Front 11

What are Karl Landsteiner and Merrill Chase famous for in the 1910-1950's?

Back 11

Blood groups, antibody/antigen structure & interaction

--> Transfer of WBC contributes to immunity to M. tuberculosis in guinea pigs

Front 12

(1910-1950)
-Emil von Behring & Shibasaburo Kitasato (serum transfer provides immunity)
-Elvin Kabat (immunoglobin)

Advanced the study of (cellular/humoral) immunity.

Back 12

Humoral


(immunity via, fluid (pustule) response)

Front 13

(1910-1950)
-Elie Metchnikoff (WBC are phagocytic)
-Karl Landsteiner & Merrill Chase (transfer of WBC contributes to immunity)

Advanced the study of (cellular/humoral) immunity.

Back 13

Cellular


(immunity via response from specific cells located w/i body)

Front 14

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?

Back 14

a) 1950's

b) Tolerance (body stops developing response)

c) Clonal Selection theory (# cells in body expands)

Front 15

T/F

Generation of diversity encompasses both germline and somatic mutation theory.

Back 15

True!


(immunity is both inherited (germline) & developed from lifetime exposure/experience (somatic))

Front 16

In the 1950's to present, Jerne, Edelman, Milstein & Kohler, Zinkernagel & Doherty, Benacerraf, and Tonegawa have contributed to the study of what?

Back 16

Cellular and molecular explanations of immunological events

Front 17

What are the general pathogens encountered by our immune system?

Back 17

Bacteria (prokaryotes)
Viruses (non-cellular)
Fungi (eukaryotes)
Parasites: protozoa (eu) and helminths (eu)

Front 18

Which pathogen type is not a cell (CANNOT survive w/o host)?

Back 18

Virus

(NEITHER prok or euk)

Front 19

Which pathogen type is the smallest? the largest?

Back 19

Smallest - virus (.02-.2 micrometer)

Largest - protozoa/helminth (15-25 micrometer)

Fungi - 3-10
Bacteria - 1-5 (smallest living)

Front 20

Main diff btwn prokaryotes & eukaryotes

Back 20

prokaryotes:
-bacteria ONLY
-no mitochondria
-replicate via binary fission

eukaryotes:
-fungi, protozoa, helminths
-membrane bound nucleus
-have mitochondria

Front 21

Which entry routes into the body are mucosal surfaces?

What is the purpose of mucus?

Back 21

airway, GI tract, reproductive tract

Mucus continually bathes mucosal surfaces, protecting the epithelial cells and limit infection.

Front 22

a) What entry routes into the body consist of external epithelia?

b) What is the purpose of skin against pathogens?

Back 22

a) External surface, wounds and abrasions, and insect bites

b) Skin forms a tough, impenetrable barrier of epithelium protected by layers of keratinized cells

Front 23

T/F

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

Back 23

False!

Innate response occurs FIRST (usually contains infection)
THEN if a threshold level of antigen/ microorganism is present, to the adaptive immune response is activated

Front 24

What occurs after the adaptive immune response?

Back 24

immunological memory if formed

(= faster response next time)

Front 25

Differentiate btwn Innate & adaptive immunity


Which includes cell-mediated (T cell) & humoral (antibodies) immunity?

Back 25

Innate= inherited

adaptive= acquired during lifetime by exposure

Adaptive immunitt

Front 26

What 2 things does the clearance of pathogens depend on?

Back 26

1. microbial recognition
(by antigen presenting cells (Dendritic cells, macrophages, and B cells)

2. Immediate response of effector cells
(destroy & eliminate the pathogens (neutrophils, macrophages, NK cells, and effector T and B cells)

Front 27

Epithelial cells joined by tight junctions (skin), air/fluid flow, & cilia movement of mucus are (mechanical/chemical/microbiological) components of the innate immune system.

Where is this defense located?

Back 27

Mechanical

Skin, gut, lungs, eyes/nose

(skin water proof, renewed every 15-30 days)

Front 28

Lactic acid, fatty acids, low pH, enzymes, surfactants A & D, & antibacterial peptides are part of the (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?

Back 28

Chemical

Skin, gut, lungs, eyes/nose

Front 29

How do Surfactants A & D protect against pathogens?

Back 29

They function as opsonins, which enhance the efficiency of phagocytosis

(lungs)

Front 30

How does lysozyme (salivary enzyme) protect against pathogens?

Back 30

It is a hydrolytic enzyme and cleaves the peptidoglycan layer of the bacterial cell wall

(eyes/nose)

Front 31

How do antibacterial peptides (defensins) protect against pathogens?

a) Where is alpha-defensin made?
b) Where is beta-defensin made?

Back 31

Defensins kill bacteria, fungus and enveloped viruses by perturbing their membrane.
(skin/gut/lungs)

a) cryptidine made by paneth cells of the small intestine

b) epithelial cells of the epidermis, GI and respiratory tract

Front 32

Normal flora is an example of a (mechanical/chemical/microbiological) component of the innate immune system.

Where is this defense located?

Back 32

Microbiological

Skin and gut

Front 33

How does normal flora defend against pathogens?



What are some examples of normal flora?

Back 33

It competes with them for nutrients and attachment sites on epithelial cells

S. aureus, S. epidermidis, Streptococcus species, Propionibacterium, E. coli, etc.

Front 34

T/F

Cytokines, chemokines, & complements are also cell mediators involved in the innate immune system

Back 34

FALSE

NOT cells
cytokines & chemikines= small peptides released from cells to work on other cells
complements= coenzymes & enzymes normally present, enhance phagocytosis

Front 35

What on the cell surface of innate immunity cells (ex, macrophages), is responsible for recognizing pathogens in the innate immune response?

Back 35

Pattern Recognition Receptors (PRR)

several structural types, can bind to a diverse array of ligands including peptide, proteins, glycoproteins, peptidoglycan, carbohydrate, glycolipids, phospholipids, and nucleic acids.

Front 36

Germline encoded receptors (PRR), recognize a specific pattern or molecular signature of a particular group or organism. What is this called?

Back 36

Pathogen associated molecular pattern (PAMP)


(PRR recognize specific patterns NOT specific pathogens)

Front 37

Mannose receptors are specific for what?

Back 37

Fungi

Front 38

LPS receptors and Toll (TLR4?) receptors are specific for what?

Back 38

Gram negative bacteria

Front 39

Inflammation is a coordinated response (1st response after recognition) to cell injury characterized by what 5 things?

Back 39

Heat (calor)
pain (dolor)
redness (rubor)
swelling (tumor)
sometimes loss of function

Front 40

What induces inflammation?

Back 40

A variety of inflammatory mediators released as a consequence of pathogen recognition by macrophages - cytokines, complements, PGs, leukotriens, and platelet activating factor.

Front 41

What do inflammatory mediators (cytokines, complements, PGs, leukotriens, platelet activating factor) all function together to do?

Back 41

1. Deliver effector molecules & 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

Front 42

What is released by injured tissue? What is activated?

Back 42

Releases cytokines, chemokines, and other mediators.

Activates complements.

Front 43

What induces dilation of blood capillaries in inflammation?

What does this cause?

Back 43

Cytokines

This causes increases blood flow, making the area red and warm

Front 44

What increases cell recruitment (neutrophil, macrophage) to the site of injury?

How?

Back 44

Cytokines and chemokines

By upregulated adhesion molecule expression on the endothelium.

These cells present at the site of inflammation are called inflammatory cells

Front 45

What happens when vasodilation induces gaps between the endothelial cells?

Back 45

increased leak of blood plasma into the interstitial cells, causing a local increase in fluid volume -> edema or swelling

Front 46

What causes the pain during inflammation?

Back 46

The increase in fluid volume (edema) puts pressure on nerve endings. PG, one of the inflammatory mediators, is also a potent pain inducer!

Front 47

It benefits the host that inflammation calls upon a (immediate/delayed) engagement of the host-immune response.

Back 47

immediate

-->in most of the cases contains the infection.

Front 48

In the innate immune response, macrophages engulf the pathogen and produce what?

Back 48

Cytokines and chemokines,
which induce a local inflammatory response.

Front 49

Why does the innate immune response recruits neutrophils and NK (natural killer) cells to the site of infection?

Back 49

To enhance the immune response

Front 50

What is the function of complements in the innate immune response?

Back 50

-act as a molecular tag & enhance the performance of effector cells
-also form protein complexes to damage the pathogen cell membrane (membrane attack complex).

Front 51

Innate immunity is (fixed/adaptive) and adaptive immunity is (fixed/adaptive).

Back 51

Fixed (innate)

Adaptive (adaptive DUH)

Front 52

Innate immunity is (slow to develop/immediate) and adaptive immunity is (slow to develop/immediate).

Back 52

Immediate (innate)

slow to develop (apadtive)

Front 53

Innate immunity is (specific/non-specific) and adaptive immunity is (specific/non-specific).

Back 53

Non-specific (innate)

specific (adaptive)

Front 54

Innate immunity (does/does not) have immunological memory,
and adaptive immunity (does/does not) have immunological memory.

Back 54

Does not (innate)

does (adaptive)

Front 55

Innate immunity (does/does not) have self and non-self discrimination,
and adaptive immunity (does/does not) have self and non-self discrimination.

Back 55

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.

Front 56

Which is more diverse - innate or adaptive immunity?


Which involves lymphocytes (T & B cells)?

Back 56

Adaptive


adaptive

Front 57

What happens if the innate immune response fails?

Back 57

Adaptive immune response takes over

Front 58

Antigenic component receptors on (T/B) cells
undergo somatic hypermutation.

BOTH T & B cells have receptors that undergo random somatic recombination

Back 58

B cells

Front 59

Ig (on B cells) & T cell receptor (TCR) (on T cells) recognize & bind molecules, macromolecules, virus particles or cell that contains a structure specific for them.
What are these particles collectively called?

Back 59

Antigens

Front 60

What is the particular part of the antigen bound by the Ig or TCR called?

Back 60

Antigenic determinant or epitope

Front 61

T/F

The interaction between antigen and Ig or TCR is specific.

Back 61

TRUE

(each B & T cell can ONLY bind ONE specific antigen)

Front 62

a) Ig (B cell receptor) is formed by (#) different polypeptides. What kinds of chains are these?

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

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

Back 62

a) 2, heavy & light chains

b) Variable region

c) Constant region

Front 63

What are the 5 different Ig isotypes?

What are their differences based on?

Back 63

IgM, IgD, IgG, IgA, IgE

On the basis of different constant regions

(Cell surface antigen receptors have IgM & IgD)

Front 64

Antibodies are secreted Ig's, lacking what region?

Back 64

Transmembrane region

(antibody + transmembrane = B cell)

(T cells are ALWAYS membrane bound)

Front 65

How many chains are in a TCR (T cell receptor)?
What are the types?

Back 65

2, alpha and beta chains

(both anchored in T cell membrane, both have a variable & a constant region, variable region forms antigen binding site)

Front 66

What determines the availability of a pathogen-specific receptor on a lymphocyte?

Back 66

It is genetically determined and occurs at random

Front 67

T/F

Selection of a receptor on lymphocytes by a pathogen depends on the availability of the receptor specific for that pathogen.

Back 67

True!


(No receptor available = no detection)

Front 68

T/F

Receptors on lymphocytes are germline encoded.

Back 68

True!

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

Front 69

T/F

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

Back 69

False!

Each cell carries 1 type of receptor specific for any particular Ag

Front 70

When are effector cells produced & what do they do?

Back 70

encounter of a lymphocyte receptor w/ specific Ag (antigen)--> signaling cascade =
Proliferation & differentiation of lymphocytes --> produces a clone of effector cells (clonal selection)-->

Effector cells are equipped with the ability to kill pathogens, directly or indirectly.

Front 71

What is the key principle for developing a diverse but specific adaptive immune system?

Back 71

Clonal selection

Front 72

Rearrangement of different gene segments of Ig and TCR in the soma is called what?

Back 72

Somatic recombination

Front 73

What are the different ways that diversity is created between Igs and TCRs (allowing specificity to billions of pathogens)?

Back 73

- rearrangement of germline DNA segments
- somatic recombination
->alternative forms of genes encoding the variable regions can rearrange in numerous different combinations
--> various combination of light and heavy chains in Ig molecules

Front 74

What is junctional diversity

Back 74

addition of new nucleotides at the junction of V region gene segments result in additional diversity of hypervariable region

Front 75

(ONLY FOR Ig)
After encounter with pathogen, activated B cells in secondary lymphoid tissue undergo process involving nucleotide substitution into Ig heavy & light chain genes. What is this process called?

Back 75

Somatic hypermutation

Front 76

(ONLY for Ig)
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?

Back 76

Affinity maturation

Front 77

T/F

B (Ig/Abs) & T (TCR) cells recognize the same things

Back 77

FALSE

TCR recognizes processed short peptides ONLY

Abs recognize bacteria, virus, toxin & bind to pathogen surface

Front 78

a) TCR ONLY binds short peptides presented to them in a complex w/ a membrane glycoprotein called what?

b) What are these short peptides derived from?

Back 78

a) major histocompatibility complex (MHC I or II)

b) derived from the breakdown of the pathogen molecule within the cell expressing the MHC molecules

Front 79

Cells that present peptides to the TCR are called what?

Back 79

Antigen-presenting cells


(process of antigen presenting = antigen processing)

Front 80

Small peptide fragments from degraded viruses or intracellular bacteria (that reside in the cytosolic vesicles) are bound to _______ in the ER (after being degraded to smaller peptide fragments)

Back 80

MHC class 1 molecule

Front 81

Peptide fragments bound to MHC 1 are transported to the cell surface & recognized by what?

Then what happens?

Back 81

CD8 T cells (cytotoxic T cells)


CD8 T cells will kill the virus-infected cell!

Front 82

Peptide fragments from degraded extracellular pathogens are bound to MHC 2 & transported to the cell surface and recognized by what?

Then what happens?

Back 82

CD4 T cells (helper T (TH1 or TH2) cells)


CD4 T cells interact with APC & augment their functions

Front 83

(B cells/macrophages) interact with TH1 cells, while (B cells/macrophages) interact with TH2 cells.

Back 83

Macrophages -> TH1

B cells -> TH2

Front 84

What are the 3 functions of antibodies?

Back 84

Neutralization- bind & neutralize pathogens & toxins

Opsonization- IgG coats bacterial surface & facilitates phagocytosis

Complement activation- activate complement which opsonizes pathogen

Front 85

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?

Back 85

Opsonization by complement activation, because phagocytes do not have a receptor for IgM constant region

Front 86

Thymocytes with different TCR interact with MHCI & MHCII molecules on cortical epithelia.

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

b) Next, 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?

Back 86

a) Positive selection

b) Negative selection

(note: T-cells originate in bone marrow--> thymus)

Front 87

What happens to clones of B cells with Ig receptors that bind strongly to bone marrow constituent cells?

Back 87

Eliminated by induction of apoptosis
(programmed cell death)

Front 88

How does the secondary response (of antibody and effector T cells) to an infection compare to the primary response in duration and intensity?

Back 88

The secondary response occurs in much shorter time with a significantly greater intensity.= memory

*This principle underlies the success of vaccinations

Front 89

(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.

Back 89

TH2

TH1

Front 90

What do cytotoxic T cells (CTL) do?

Back 90

Kill virally infected cells

Front 91

What happens when you lack innate immunity?

Back 91

Uncontrolled infection, as adaptive immunity can not be deployed without preceding innate response

Front 92

What happens when you lack adaptive immunity?

Back 92

Initially controlled by innate immunity, but it will fail to clear eventually

Front 93

Host immune system responds to inoculous substances in the environment, usually secondary response when re-exposure to an Ag causes the Ag to bind to an IgE Ab (formed from previous exposure & bound to receptors on mast cells via constant region)
What is this condition?

Back 93

Allergy or hypersensitivity

Front 94

Ag binding to IgE Ab leads to degranulation of mast cells (releasing histamine, cytokines, leukotriens, bradykinins, etc).
These mediators may give rise to severe life threatening conditions such as what?

Back 94

Acute bronchial asthma and systemic anaphylaxis

Front 95

Development of insulin-dependent diabetes mellitus (IDDM) has been correlated with previous infection with what?

Back 95

Coxsackie virus

Front 96

Why do symptoms appear later in IDDM?

Back 96

Healthy pancreas can make much more insulin than required, symptoms won't appear until 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.