Ntc 4: Immune System 1

Front 1

type of immune cells

Back 1

1-2

Front 2

Maturation of B-cells

Back 2

within the sinus: antigen is encountered> it reacts at the primary focus* and plasma cells start to become specific in antibody production (IgM)> in the germinal centre* b cells undergo affinity maturation* and isotype switching* they start making IgG, IgD, IgE

Front 3

Anitbody productions

Back 3

still talking about B cells
class switching: antibody changes class but retains affinity for the same antigens. Now it can just interact with different effector molecules

Affinity Maturation: the process by which b cells produce antibodies for antigen

Front 4

antibody effector functions

Back 4

neutralization, opsonizations and phagocytosis, antibody dep cytotoxicity, complement activation (lysis of microbes, phagocytois of opsinized microbes, inflammation)

Front 5

t cells

Back 5

T cell dependent response- Th2 helper cell interacts with a B cell. B cell matures into a plasma and secretes antibodies

T cell independent response: B cell maturation does not involve the T cell; plasma cell secretes antibodies

Can have CD4 (Th1, Th2, Th17) = cause cytokine secretion and inflammation
or CD8 (cytotoxic t cell): causes cell death

Front 6

maintaining self tolerence

Back 6

Treg cells are the main guys that inhibit self-reactive T cells

self reactive clones react with thymic epithelial cells, this induces apoptosis and are removed

Front 7

TH1, TH2, TH17: cytokine reg of T-cell type

Back 7

T-cell type is controlled by transcription factors that act differently on these cells

th17 prod IL 17

Th2 prod IL4 (eosinophils) Il 4 inhibits th17

Front 8

MHC 1 and 2

Back 8

every nucleated cell expresses MHC 1, when they dont they are destroyed
antigen presenting cells express MHC 2

Front 9

apoptosis

Back 9

Nk cells are attracted to site of infection by gradient of soluble cytokines

the nk cells express Fas ligand and the target cell expresses the Fas receptor. they bind= apoptosis

Front 10

innate immune response

Back 10

has PRRs(this includes TLRs which recognize bacteria and viruses) for PAMPs

Cytosolic PRRs are used mainly for viruses

Front 11

What is the relevance of giving wild mice hep and mice lacking adaptive immunity hep?

Back 11

the lab mice die bc they lace the CD4 t cells to inhibit TNF alpha over production. this causes immunopathology death

Front 12

NLRs

Back 12

nucleotide binding prot
can activate the inflammasome complex and other things
main function: intracellular cellular sensing of PAMPs
these guys are associated with genetic immunological disorders

Front 13

dendritic cell directly infected by virus rec pamps (intracellular)

Back 13

viral pamp is located w/in the dendritic cell. it reacts w/ RIG system which signals to the nucleus and causes release of cytokines and co-stimulatory molecules

both MHC 1 complex and MHC 2 complex are produced at the surface

Front 14

microbiota of the gut

Back 14

see pg 7

ReglllA, clostridia, bacteroides fragilis

inner gut protected by: IgA, RegIIIy ...

Front 15

what's the difference b/w early and late infection of the gut?

Back 15

E: increase in virulence factors released by back, inflammation, damage to epithelium

L: decrease in virulence factors, change in microbiota struct, competition for nut, pathogen clearance (your good to go)

Front 16

Dysbiosis

Back 16

condition of microbial imbalance,
- changes is the balance of inflammatory bac (PRO + ANT) lead to disease such as MS, diabetes, crohns...
-normally in the gut, B gragillis and SFB are in balance. this results in the balance of Treg and Th17

+ pro inflam bac (sfb) can lead to increase in TH17 cells and inflammation in the colon
- anti inflam bac (B fragillis) leads to a decrease in t reg cells and inflammation of the colon

Front 17

Diabetes 1

Back 17

new evidence suggests that neutrophils produce CRAMP which acts with self DNA (from damaged cells) this then stimulates pDC to produce interferon, which stimulates the cDC (conventional) to present a self peptide

Front 18

diabetes type 2

Back 18

abs of defective TLRs in the gut change the microbiota and result in increased food intake and insulin resistance

Front 19

bac on an epithelial surface: response

Back 19

extracellular bac stim dendritic cells and Th17 cells which both secrete Il22. this stim the epithelium to produce STAT3 (causes epithelial repair and antimcrobial prot)

th17 also secreter IL17 which recruits neutrophils, Il22 promotes repair

Front 20

MyD88

TcpC

Back 20

M: causes activation of transciption factors to initiate trans of gens for the host d mech (in e coli)

T: e coli for uti

Front 21

Hypersensitivity rxn type 1
anaphalatic

Back 21

anaphylactic (IgE)

- modulated by Ige (usually used for parasites), they activate the mast cells (via cross linking)

-immediate resp: hist causes vaso dialation, vasc leakage, and constriction of smooth musc aroung the lungs/nose
-Late: leukocyte infiltration, epithelial damage, bronchospasm

*sarafotoxins binds to receptors on the mast cell and causes the ER to release Ca, increase intracellular ca causes degranulation. CPA is relased, which destroys the toxin.
Worms produce ES-62 which blocks TLR on mast cells and prevents degranulation

Front 22

type 1
hayfever

Back 22

allergic inflammation of the nasal airways and caused by inhaled allergens

1st exposer: Il4 of t cells drives b cells to produce IgE in response to pollen antigents, pollen specific IgE binds to mast cell
2nd exposer: acute release of mast cell contents causes allergic rhinitis

ppl use sodium cromoglycate (blocks both phases) and indomethacin (blocks late phase)

Front 23

Cholera toxin

Back 23

WTF is the relevance of this?

Front 24

type 2: antibody dependent (cytotoxic)

Back 24

antibody (non-IgE) binds to an antigenic surface by Fab segments
carpet of antibodies attract wbc and activates complement thereby attracting more wbc

Front 25

type 2: Hemolytic anemia

Back 25

can be antibody dependent (c5-9 form membrane attack complex and causes lysis, Fc receptor on macrophage undergoes phagocytosis mediated by opsonization) blood type or Rh incompatability

Front 26

what are the classes of allergic rxns?

Back 26

fsdfsd

Front 27

type 2: myasthenia gravis

Back 27

antibodies to Ach receptor blocking ability of acetylcholine to act on receptors of muscles

Front 28

type 3: immune complexes

Back 28

pg 12

Front 29

type 4: cell mediated, contact dermatitis, sympathetic ophthalmia

Back 29

pg 13