Quiz 2 Immunity

Question 1

Innate immunity pathway

Answer 1

Dendrite/Macrophage’s TLR recognizes PRR/PAMP and stimulated macrophages (phagocytize), inflammatory cytokines (inflammation/shock), and interferons (antiviral)

Question 2

Adaptive immunity pathway

Answer 2

Dendrite/APC “Eats” and processes an antigen, presenting it on MCH I/II via IL12 & 4 pathway —-> Tcell’s TLR binds MHC I (Th1) or MHC II (Th2) and activates via costimulation from B7 (APC) and CD28 (Tcell) bonding —-> IL-12 pathway differentiates Th1 cells, IL4 pathway differentiates Th2 —-> Th1 uses IL-2 to diff into CD8 (Cytotoxic T cells) and INF-y to diff into macrophages. Th2 uses IL4,5 to diff into B cells, and CD4+T (helper Tcell) initiates Bcell activation via CDL40 (CD4+T) and CD40 (Bcell) binding, CD4+T secretes cytokines to stimulate B cell class switching to change Ig into IgM (aka mature B cells) then B cells can differentiate into plasma cells and make antibodies

Question 3

B cell activation & class switching

Answer 3

After the naive Tcell differentiates into Th2/CD4+T (via IL-4 pathway) to activate Bcells, it recognizes Bcell’s TLR and makes IL4 (growth) & IL5 (differentiation) factors to make more Bcells —> then CD4+T activates Bcells via CDL40 (T)—–CD40(B) & CD28(T)—-B7(B) Bonds to trigger cytokines from CD4+T to trigger Bcell class switch from Ig to IgM (mature Bcells that can differentiate into plasma cells and make antibodies)

Question 4

Hapten-Induced Bcell activation

Answer 4

Carrier proteins let haptan’s epitope bind with the hapten-specific IgM on Bcells —-> the epitope interacts with CD4+T’s TLR & Bcell’s MCHII to stimulate more IL4 (Growth) & IL5 (Differentiation) to increase Bcells and antibody-producing plasma cells

Question 5

Immuno globin structure

Answer 5

2 heavy & 2 light chains are linked via disulfide bonds, and it has a

Fab (fragmented Antibody Binding)= has the variable region, and it determines the isotype (Ig__)

&

Fc (Fragmented Crystallizable) parts, include constant region, carboxyl-terminal, CH2 complement binding site, CH3 site for binding macrophage and neutrophil receptors, confers isotype (Ig____)

Question 6

Immunoglobulin classes

Answer 6

IgG (H2L2) = Transplacental (mom—> fetus) IgG fixes the compliment, opsonizes the bacteria, then neutralizes the bacterial toxins/viruses. Has subsets Ig1-4 (1 has longest 1/2 life & Is most important)

IgA (H2L2)= Secretions, polypeptides move IgA to mucus membranes and prevent attachment by microbes, serum IgA = x2H2L2, IgA protease disrupts IgA and leaves host vulnerable

IgM= Is active in the primary (immediate) immune response; it’s on Bcells as monomers that act as antigen receptor binding surface receptors. It fixes the compliment. In serum, IgM = pentamer (x5 H2L2 & 10 antigen binding sites) increases its avidity to defend against bacteria/viruses.
- It’s most efficient in AGGN (complement fixation/activation pathways)
- associated with certain fetal infections and cold autoimmune hemolytic anemia

IgE = involved in the immediate hypersensitivity reaction (allergy) because its Fc binds to Mast + Basophils, and IgE cross-links with the antigen (increases serum IgE). IgE also recruited eosinophils to improve the host’s defense against parasites. Lastly, IgE initiates ADCC (Antibody-dependent cellular cytotoxicity)

IgD= not sure yet, but its on Bcells in serum and might be an antigen receptor

Question 7

Serum vs. Anti-serum vs. Serum sickness

Answer 7

serum = the fluid left over after clotted blood and cells are removed

antiserum = apart of the serum with the highest concentrations of antibodies

serum sickness= multiple injections of serum cause disease and illicit a systemic immune response (type 3 hypersensitivity) against proteins and cause an Arthus reaction (local inflammation at injection site looks like a target) treat with epi/nore epi or die from shock

Question 8

Consequences of the antigen-antibody binding complex “AC is Always ON All Day, it Costs Alot”

Answer 8

Agglutination= antibodies cause antigens to cluster. (IgM is most efficient)

Opsinization= antibodies coat an antigen and increase chances of being phagocytized.

Neutralization= Antibody binds & blocks the active site on a virus, inactivating it and neutralizing its toxins (IgG is best)

ADCC (antibody-dependent cell-mediated cytotoxicity)= antibodies bind to a larger antigen (parasite) and recruiter eosinophils to destroy it (IgE is best)

Complement activation= antibodies trigger the complement pathway (IgG & M are good)

Question 9

Bcell class switching is also called

Answer 9

isotype switching

Question 10

B & T cells that don’t undergo CD28—-B7 bonding are considered

Answer 10

incompetent and anergic (can’t metabolize ATP to function)

Question 11

MHC I, II, & III

Answer 11

MHC I= HLA A,B,C

MHC II= HLA DQ, DR, DP

MHC III= C2,3 BF

Question 12

Idiotype vs. Allotype vs. Isotype

Answer 12

Idio = differences in the epitopes of the hypervariable regions of light and heavy chains (increase in diversity of receptors)

Allo = minor differences in the constant regions of the heavy chain (IgG1 —-> IgG4)

Iso = differences in the heavy chains that lead to several antibody classes (class switching)

Question 13

Affinity vs. Avidity

Answer 13

Affinity = strength of one bond (between the para & epitope), it has high specificity (IgG has high affinity)

Avidity = strength of multiple bonds (IgM is a pentamer and has high avidity but low affinity)

Question 14

If your patient has recurrent viral infections it means they have

Answer 14

depleted NK cells (NK cells use IgG)

Question 15

Cell-mediated immunity is also called

Answer 15

type 4 hypersensitivity or DTH (deleted type of hypersensitivity)

Question 16

Rogue cells cause

Answer 16

nut-dishevelled signaling (uses hosts resources but acts on its own accord)

Question 17

Positive vs. negative selection (thymic education of Tcells)

Answer 17

Positive= happens in the thymic cortex, it eliminates Tcells that do NOT recognize MHC complexes on our own cells (i.e Don’t recognize self)

Negative = happens in the thymic medulla, it eliminates Tcells that DO recognize our self antigens (this prevents autoimmune reactions aka friendly fire)

Question 18

What is the role of CD3?

Answer 18

it helps intracellular signaling and activating transcription factors that give rise to the JAK-STAT pathway (produces cytokines)

Question 19

Graft vs. host disease

Question 20

immunogens response can be boosted by which drug

Answer 20

penicillin

Question 21

Winter Bottom sign?

Answer 21

enlarged cervical lymph nodes that might indicate an active infection

Question 22

Natural killer cells (null cells) are involved in

Answer 22

innate immune response to viruses and cancers, they also double as immune surveillance
and use CD16 (ADCC) & 56 (interact with IgG’s via FC bonding to kill cancer) as biomarkers to differentiate friend from foe

Question 23

IL1,2,3,4,5,6,7,8,

Question 24

3 Stages that lead to higher specificity of adaptive immunity in terms of high affinity bonding are

Answer 24

Class-switch recombination—–> somatic hypermutation—–> affinity maturation (this is why our adaptive immunity has a lag period as opposed to our innate defenses)

Question 25

Types of hypersensitivity reactions 1,2,3,4

Answer 25

Type I (immediate/anaphylactic) = Minutes long; it’s mediated by IgE.

Sensitization –> happens when first exposed to an antigen because it causes IgE to be synthesized and bind to Mast/Basophils
Reaction –> when exposed to the antigen a second time, it binds to IgE forming AAC’s which, along with Ca, trigger the release of mediators (histamine, etc) from Mast/Basophils, causing edema + erythema

Immediate phase happens in minutes & Late phase happens after ~6hrs

“FAst Allergies Do HUrt”: Food, asthma, anaphylaxis, Drugs (esp penicillin), Hives/Urteria

Type II (cytotoxic) = hrs-to-days long; it’s mediated by IgM/IgG

Sensitization –> Exposure to an antigen causes IgE to bind to cells (become cell-fixed)
Reaction —> The antigen binds to IgE (forming AAC) and activates the complement pathway for cell lyses

“Two GP’S Have Many Graveyard HRs”: Good Pasture’s syndrome, Hemolytic anemia, Myasthenia Gravis, Graves disease, Rh incompatibility

Type III (Toxic/immune complex) = Days-to-weeks long, mediated by IgM & IgG

Sensitization –> circulating antibodies bind to antigens to form ACC’s
Reaction —> ACC’s are deposited into tissues (esp basement membranes of kidneys/lungs) and activate the complement pathway to cause inflammation and tissue damage

“Erd ReAction KiLSS”: Serum sickness, Arthus reaction, Rheumatoid arthritis (IgM attacks IgG), Kidney failed (cause of death), Systemic Lupus, Erythromatoses

Type IV (Cell-mediated/Delayed): 2-3 days long; it’s mediated by T cells

Sensitization –> Tcells encounter an antigen
Reaction –> A delayed reaction where memory T cells recognize the antigen via MHC II and trigger CD8 T cells to release Cytokines, differentiate into NK cells, & recruit macrophages/eosinophils

“Delayed Tcells Lure Phagocytotic Macrophages”: Dermatitis, TB skin test, Latex, Poison Ivy, Metals

Question 26

Acute vs. Chronic desensitization

Answer 26

Acute –> injecting small amounts of antigen to illicit a minor response at 15 minute intervals (a temporary fix usually to inject drugs that people are allergic to)

Chronic –> Stimulating IgA + IgG’s to block the active site on Mast/Basophils from IgE & inducing regulatory T-cells to make more IL-10 to reduce IgE production

Question 27

Good Pasture’s syndrome

Answer 27

The AAC from the type II hypersensitivity reaction is deposited in the basement membranes of the lungs and kidneys, the activated complement pathway leads C5a (chemotactic factor) to attract leukocytes to damage the membranes.

Question 28

Alternative Hypersensitivities:
Jones Mote Hypersensitivity “THAnks Very Much JONES”
Contact Hypersensitivity

Answer 28

Jones-Mote= Soluble antigens induce overactive Basophils under the epidermis against viral antigens, tumors, hypersensitive pneumonitis (farmers lung), and allograft graft rejection

Contact= max 48hrs, an epidural reaction where Langerhans cells are the APC’s

Question 29

Endogenous vs Exogenous MHC pathways

Answer 29

Endo= MHC I (CD8) All nucleated cells
Exo= MHC II (CD4) APC’s only

Question 30

T-cell dependent Ag

Answer 30

TCD-Ag + CD4’s = Bcell activation and specific antibodies to epitopes

APC’s (TCD-Ag) + MHC II bind TLR of CD4 —> CD4 (TCD-Ag) then binds to Bcell, whose surface receptors at sites complementary to the epitope capture and process the TDC-Ag —> Bcell’s endogenous MHC II presents the TCD-Ag to prime other Tcells to release cytokines that will make plasma cells produce epitope-specific antibodies