FINAL REVIEW part 3 - immune system/hypersensitivity/autoimmune

Question 1

Innate immunity components?

Answer 1

(Also called Cellular): Skin, epithelial barriers, phagocytes, dendritic cells, NK cells (innate action of what specific CD8+ cells do), complement system

Question 2

Adaptive immune system component?

Answer 2

(Also called humoral reponse):
B-lymphocytes ->PLasma->Ig
APC->T-lymphocytes->Effector T cells

Question 3

Blood clot last steps?

Answer 3

Thrombin ->fibrinogen into fibrin

Question 4

Dendritic cells in the skin called?

Answer 4

Langerhans cells

Question 5

MHC class 2 present on?

Answer 5

APC:dendritic, macro, B cells

Question 6

Factors released by dying cells are called?

Answer 6

Death-Associated Molecule Patterns (DAMPs)

Question 7

What make the difference between recognizing MHC class 2 or 1 by T cells?

Answer 7

Co-receptors:
CD4 - MHC class 2 = T helper cells
CD8 - MHC class 1 = Cytotoxic T cells: 1)Expression of FAS ligand, inducing apoptosis. Then, Release perforins allowing granzymes to trigger caspase cascade leading to apoptosis
Co-stimulatory molecule = CD28

Question 8

Central tolerance?

Answer 8

Suppression of lymphocyte that react to strongly to self:
Bcell: in bone marrow
Tcell: in Thymus

Question 9

Peripheral tolerance

Answer 9

Suppression of lymphocyte that react to strongly to self .

Question 10

2 ways B cell can be activated?

Answer 10

1) T-cell independant: Microbe binds directly to surface Ig and triggers humoral response
2) T-cell dependant: Microbe binds to B-cell receptor, phagocytosed by B-cell, displayed on MHC II, T CD4+ cell bind and triggers humoral response by B-cell.

Question 11

Only cell that can activate naive t cells?

Answer 11

Dendritic cells

Question 12

Four types?

What is hypersensitivity?

Answer 12

Type I - Immediate/allergy
Type 2 - Antibody-mediated
Type 3 - Immune complex-mediated
Type 4 - Cell-mediated

Def: Reaction by immune system that damages the body instead of protecting it

Question 13

1. Type I - Immediate/allergy mechanism?

2. Local vs systemic type I hyper.

Answer 13

1. Activation of Th2 CD4+ by envir. antigens presented by B-cells -> Th2 produce IL-4 -> B-cell class switching -> Prod. of IgE by B cell -> IgE bind to Fc Epsilom receptors on the surface of mast cells -> Antigens bind to now attached IgE and Activate Mast cell to release Histamine/other mediators
2. Local: Antigens confined (Eg. skin, git)
   Systemic = Anaphylaxis

Question 14

Type 2 - Antibody-mediated general mechanism of action?

Answer 14

Are caused by antibodies (IgG) that bind to fixed tissue or cell surface antigens, promoting phagocytosis and destruction of the coated cells or triggering pathologic inflammation in tissues.

Question 15

Type 3 mechanism of action?

Answer 15

IgG bind to soluble antigens creating a complex that will deposit itself on basement membrane of tissues -> Activating complement cascade

Question 16

Type 4

1. CD4+ mechanism of action? + can also create? +Eg
2. CD8+ mechanism of action? + Eg

Answer 16

1. Delayed-type hypersensitivity (24hours+): Naive T-cell differentiate into either Th1 or Th17 after presentation of antigens by dendritic cell -> upon 2nd expose the memory T-cell Th1 will release IFNgamma (Th17 - IL17) -> activating macrophage -> they release proinflammatory mediators -> causing tissue damage
   Can also create granulomas.
   Eg: Poison Ivy -> Urushiol (hapten)
2. CD8+ recognize antigens on MHC class 1 as non-self and destroy the cell.
   Eg: DM type1 => Attack beta-cell in pancreas (secrete insulin), leave alone alpha cell (glucagon)

Question 17

Type 2, 3 specific mechanism of actions?

Answer 17

1) Phagocytosis: IgG bind to cell/activate complement and phagocytes eat the target cell
2) Inflammation: C5a and C3a lead to recruiment of neutro and causing inflammation.
3) Blocking receptor function: (Eg. Graves disease, Ig bind to TSH receptor stimulating thyroid cell to produce T4/T3, resulting in hyperthyroidism.)

Question 18

Type 2 Eg/

Answer 18

1) Graves disease, Ig bind to TSH receptor stimulating thyroid cell to produce T4/T3, resulting in hyperthyroidism.
2) Myasthenia gravis: Ig bind to Ach receptor blocking Ach stimulation of musc.
3) New born hemolytic anemia: mother Rh-/Baby Rh+, first exposure mother develop anti-Rh Ig. 2nd pregancy, Ig bind to RBC of baby and initiate immune reaction.

Question 19

Reversible liver diseases?
Irreversible liver diseases?
Cells causing scaring in liver?

Answer 19

fatty, hepatitis
Fibrosis ->Cirrhosis
Stellate cells

Question 20

Pathogenesis of SLE?

Answer 20

Susceptibility genes + External triggers (UV light) ->apoptotic bodies -> Ig against apoptotic bodies -> (type 3 hypersensitivity)

Question 21

Rheumatoid Arthritis (RA) pathogenesis?

Answer 21

{Susceptibility genes (HLA)} + {Envir. Factors that may trigger the conversion of arginine to citrulline (citrullination)} -> creation of anti-citrullinated protein ab (antibody) and other autoantibodies (all of them called rheumatoid factor)
RANKL and expressed on T cells stimulating bone resorption by osteoclast.

Question 22

Multiple sclerosis (MS) pathogenesis?

Answer 22

T cells/monocyte cross the BBB by expressing the right combination of integrins -> Diapedisis -> They then attack oligodendrocytes (making myelin sheath) -> Discoloration of white matter in the brain

Question 23

Inflammatory Bowel Disease (IBD) types?

Answer 23

Crohn’s: throughout GIT in discontinuous matter, lesion into musc. layer. Th1. NOD2 (gene) - defective = defective epi. barrier
Ulcerative colitis: Only colon, only mucosal layer. Th2. Perinuclear anti-neutrophil cytoplasmic antibodies (pANCA).

Question 24

“Transplant”, 2 types of reactions?

Answer 24

1-Direct alloantigen recognition: Host recognize MHC on graft as non-sefl. Scene of battle vasculature.
2-Indirect alloantigen recognition: Graft cells react. Scene of battle = skin,GIT,liver

Question 25

Secondary immunodeficiency : AIDS pathogenesis?

Answer 25

gp120 (HIV) -> CD4 ->gp120 -> CCR5/CXCR4 coreceptors (t-cell) ->gp41(HIV) allows it to enter cytoplasm of CD4+ T-cells

Question 26

Ways HIV kill CD4+ T-cells?

Answer 26

1) Direct killing: membrane permeability defect
2) Killed by CD8+ by MHC 1 HIV antigen recognition
3) Infected CD4+ can trigger apoptosis of uninfected CD4+

Question 27

Primary immunodeficiency : What is X-linked severe combined immunod.?

Answer 27

Pro-T cell -> gamma chain not expressed, cannot become Immature T-cell.

Question 28

Primary immunodeficiency: What is X linked gamma globulemia (BTK)?

Answer 28

Pro-B cell -> Pre B cell -> Defect in tyrosine kinase, cannot become Immature B cell.

Question 29

Primary immunodeficiency: Severe Combined Immunod. (scid)?

Answer 29

Absence functional T-cell

Question 30

Proliferation of HIV?

Answer 30

RNA converted to DNA by reverse transcriptase then enter nucleus and binds to DNA of cell. Cell needs to be undrergoing proliferation.

Question 31

Infections of cns categories?

Answer 31

1. Bacterial: Purulent meningitis, abcess, neurosyphilis
2. Viral: Herpes, HIV, aseptic meningitis
3. Parasite: Cerebral malaria
4. Prion: Spongiform encephalopathies: Human=>Creutfeldt-Jacob; GSS, Kuru. Non-Human=>Mad cow

Question 32

2 categories of cell?

Answer 32

1-Neurons
2-Glial cells: 
2.1 Oligodendrocytes: myelin
2.2 Astrocytes: Caretaking
2.3 Microglial-macrophage: