Immunology Exam 2 Lectures 10-18

Front 1

Where are the genes for kappa, lamda, and heavy chain genes located?

Back 1

kappa - chromosome 2
lamda - chromo 22
heavy chain - chromo 14

Front 2

how can there be 10^8 different Ab specificity?

Back 2

Kappa chain has 200 options
lambda chain has 720 options
heavy chain has 10530 options
so with 1 light and 1 heavy chain you get about 10 million different combos
The rest comes from post transcriptional processing

Front 3

what is an immunoglobin molecule made from?

Back 3

2 identical L chains and 2 identical H chains

Front 4

What does VDJ recombinase do?

Back 4

it is a complex system of enzymes that cause gene rearrangements and lead to the VL and VH exons of Ig genes.

Front 5

What do RAG complexes do? aka junctional diversity

Back 5

RAG's are responsible for the imprecise joining of V/J and V/DJ.
a terminal deoxynucleotidyl transferase TdT randomly adds bases to ends of V/D/J segments.

Front 6

What is somatic hypermutation?

Back 6

Almost randomly introduces single nucleotide substitutions at a high rate through the rearranged V segments of heavy and light chain genes.

Front 7

Describe pro B (bone m and blood) and pre B (periphery) cell development

Back 7

Early pro B - D/J rearrangement in heavy chain
Late pro B - V/DJ rearrangement
Large Pre-B - see pre B receptor
Small Pre-B - Mu expressed on outside and V/J rearrangement

Front 8

What is expressed on an immature b-cell?

Back 8

The moment a cell begins to express a complete IgM on its surface, it is an immature b-cell.
Negative selection allows for tolerance

Front 9

What is expressed on a mature B-cell?

Back 9

Surface IgD begins to be expressed along with IgM; both have same specificity
MHC II is also expressed.
They migrate to bone marrow for Ab production after stimulation

Front 10

Isotype class switching provides Ab of the same ____1____ but different ___2___

Back 10

1 - specificity
2 - secondary activity

Front 11

how soon does prenatal immunity start?

Back 11

8 weeks b-cells first appear in the fetal liver and are produced in bone in 2nd trimester

Front 12

what happens at 10-30 weeks?

Back 12

small amounts of Ig appear in the following order
M, D, G, A

Front 13

When does active transport of maternal IgG begin?

Back 13

begins after 16th week; more than 50% occurs after 34th week

Front 14

How long does maternal IgG persist after birth in the neonate?

Back 14

persists up to 6 months

Front 15

What about vaccines in babies?

Back 15

start at 2 months old and give live vaccines at 6 months old
Child is immunologically inexperienced

Front 16

What is the next immunologic milestone?

Back 16

puberty. this is when the thymus meets its maximal size -35grams and decreases in size to about 6 grams later in adulthood

Front 17

what is the major determining factor of adult immunity?

Back 17

environmental factors are the main determinant.

Front 18

describe prevention of epthelial cell attachment

Back 18

Secretory IgA bings organisms in external sectretions and prevents their attachment to penetration of the mucous membranes

Front 19

What is an opsonin?

Back 19

any substance that enhances phagocytosis

Front 20

Ab immun mech: opsonization

Back 20

IgG +/- compliment functions as opsonin by coating microorganisms and then binding to the surface of phagocytes via Fc receptors

Front 21

Ab immun mech: complement

Back 21

IgG and IgM are both complement fixing Ab; IgM is most efficient
compliment lyses and kills microorg

Front 22

Toxin/virus neutralization

Back 22

IgG is most plentiful in serum
it binds toxin's receptor site and inhibit it's activity

Front 23

What do the beta integrins do? name 2

Back 23

LFA-1 from leukocytes
MAC-1 from macrophages
facilitate ICAM binding and are needed for tight binding

Front 24

what are 2 disease states associated with having no beta integrins

Back 24

LAD I - leukocyte transmigration problems and repeated bacterial infection
LAD II - deficiency in Siayl-lewis factor which is receptor for e/p-selectins

Front 25

What are PAMP and PRR?

Back 25

Pathogen Associated Molecular Patterns and PAMP Recognition Receptors

Front 26

What is PRR responsible for?

Back 26

PAMP recognition receptors activate innate immunity and are required for inflam.

Front 27

What transcription factors are activated by TLRs?

Back 27

TLRs activate AP-1 and NF-kappaB which are important for mediating inflam factors.

Front 28

What are additional roles for macrophages?

Back 28

important mediators of wound healing and tissue remodeling

Front 29

What is one strong chemoattractant for neutrophils and macrophages?

Back 29

N-formyl-methionine (N-FMLP)

Front 30

what are the 2 main classes of chemokine receptors in leukocytes?

Back 30

CXCR and CCR are both receptors found on leukocytes with non-specific binding of chemokines

Front 31

What is TLR-4?

Back 31

a receptor for bacterial LPS found on macrophages that activates production of inflam cytokines

Front 32

What is the role of phospholipase A2 in the inflammatory response?

Back 32

PLA2 cleaves arachidonic acid from membrane phospholipids. Free AA is then metabolized to produce inflam mediators

Front 33

What are metabolites of AA and what do they do?

Back 33

Leukotrienes and prostaglandins cause edema.
thromboxanes and prostacyclins cause and oppose vasoconstriction and clot formation respectively

Front 34

What are the characteristics of chronic inflammation?

Back 34

1 - persistent T-cell and macrophage activity
2 - incr. matrix metalloproteinases
3 - tissue destruction and elevated levels of reactive O

Front 35

What causes chronic inflam?

Back 35

genetic traits
autoimmunity due to improper development
persistant irritation or injuries

Front 36

Describe cellular mediated immunity as an inflam disease

Back 36

-Tissue damage from autoreactive Tcells and persistent macrophages
-locally produced inflam cytokines
-psoriasis and RA

Front 37

inflam disease: immune complexes

Back 37

IgG form complexes that damage capillary bed
-Ab to self or foreign
-perpetuate response
-glomerulonephritis

Front 38

inflam disease: anaphylaxis

Back 38

possibly lethal
-after 1' sensitization, 2' leads to rapid hypersensitivity
-IgE bound to mast cells or basophils are crosslinked and cause degranulation

Front 39

What NSAID only inhibits COX-1?

Back 39

Indomethicin

Front 40

What is a leukotriene inhibitor that blocks receptor and not production?

Back 40

singulair and Accolate

Front 41

What is a 5-lipoxygenase inhibitor and what does it inhibit?

Back 41

Zyflo is an asthma treatment that prevents 5-LO;
Blocks Production

Front 42

Name a SAM inhibitor and explain it

Back 42

tysabri is a Ab against VLA-4, an integrin on WBCs

Front 43

Name an antihistamine and explain its action

Back 43

Cimetidine targets the H2 histamine receptor to prevent histamine binding

Front 44

name a corticosteriod. how does it act on inflammation?

Back 44

hydrocortisone inhibits PLA2 which is the source of many inflam molecules
also inhibits tcell prod and causes apoptosis

Front 45

how do cytokine inhibitors help RA

Back 45

kineret is recomb IL-1Ralpha that blocks IL-1 binding
RA treatment

Front 46

how does enbrel work?

Back 46

Blocks TNFalpha and beta binding
suppresses large part of immune system
RA treatment

Front 47

How does remicade work?

Back 47

anti-TNFalpha Ab that prevents its binding
RA treatment

Front 48

how does methotrexate work?

Back 48

general immunosuppressant
inhibits human DNA synthesis

Front 49

why do drugs target TNFalpha as a source of inflammation?

Back 49

it's a proinflam. cytokine that causes acute phase protein expression from liver among other things
Similar to IL-6